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Researchers seek to understand post-COVID autoimmune disease risk
Since the COVID-19 pandemic started more than 3 years ago, the longer-lasting effects of SARS-CoV-2 infection have continued to reveal themselves. Approximately 28% of Americans report having ever experienced post-COVID conditions, such as brain fog, postexertional malaise, and joint pain, and 11% say they are still experiencing these long-term effects. Now, new research is showing that people who have had COVID are more likely to newly develop an autoimmune disease. Exactly why this is happening is less clear, experts say.
Two preprint studies and one study published in a peer-reviewed journal provide strong evidence that patients who have been infected with SARS-CoV-2 are at elevated risk of developing an autoimmune disease. The studies retrospectively reviewed medical records from three countries and compared the incidence of new-onset autoimmune disease among patients who had polymerase chain reaction–confirmed COVID-19 and those who had never been diagnosed with the virus.
A study analyzing the health records of 3.8 million U.S. patients – more than 888,460 with confirmed COVID-19 – found that the COVID-19 group was two to three times as likely to develop various autoimmune diseases, such as rheumatoid arthritis, systemic lupus erythematosus, and systemic sclerosis. A U.K. preprint study that included more than 458,000 people with confirmed COVID found that those who had previously been infected with SARS-CoV-2 were 22% more likely to develop an autoimmune disease compared with the control group. In this cohort, the diseases most strongly associated with COVID-19 were type 1 diabetes, inflammatory bowel disease, and psoriasis. A preprint study from German researchers found that COVID-19 patients were almost 43% more likely to develop an autoimmune disease, compared with those who had never been infected. COVID-19 was most strongly linked to vasculitis.
These large studies are telling us, “Yes, this link is there, so we have to accept it,” Sonia Sharma, PhD, of the Center for Autoimmunity and Inflammation at the La Jolla (Calif.) Institute for Immunology, told this news organization. But this is not the first time that autoimmune diseases have been linked to previous infections.
Researchers have known for decades that Epstein-Barr virus infection is linked to several autoimmune diseases, including systemic lupus erythematosus, multiple sclerosis, and rheumatoid arthritis. More recent research suggests the virus may activate certain genes associated with these immune disorders. Hepatitis C virus can induce cryoglobulinemia, and infection with cytomegalovirus has been implicated in several autoimmune diseases. Bacterial infections have also been linked to autoimmunity, such as group A streptococcus and rheumatic fever, as well as salmonella and reactive arthritis, to name only a few.
“In a way, this isn’t necessarily a new concept to physicians, particularly rheumatologists,” said Jeffrey A. Sparks, MD, a rheumatologist at Brigham and Women’s Hospital in Boston. “There’s a fine line between appropriately clearing an infection and the body overreacting and setting off a cascade where the immune system is chronically overactive that can manifest as an autoimmune disease,” he told this news organization.
A dysregulated response to infection
It takes the immune system a week or two to develop antigen-specific antibodies to a new pathogen. But for patients with serious infections – in this instance, COVID-19 – that’s time they don’t have. Therefore, the immune system has an alternative pathway, called extrafollicular activation, that creates fast-acting antibodies, explained Matthew Woodruff, PhD, an instructor of immunology and rheumatology at Emory University, Atlanta.
The trade-off is that these antibodies are not as specific and can target the body’s own tissues. This dysregulation of antibody selection is generally short lived and fades when more targeted antibodies are produced and take over, but in some cases, this process can lead to high levels of self-targeting antibodies that can harm the body’s organs and tissues. Research also suggests that for patients who experience long COVID, the same autoantibodies that drive the initial immune response are detectable in the body months after infection, though it is not known whether these lingering immune cells cause these longer-lasting symptoms.
“If you have a virus that causes hyperinflammation plus organ damage, that is a recipe for disaster,” Dr. Sharma said. “It’s a recipe for autoantibodies and autoreactive T cells that down the road can attack the body’s own tissues, especially in people whose immune system is trained in such a way to cause self-reactivity,” she added.
This hyperinflammation can result in rare but serious complications, such as multisystem inflammatory syndrome in children and adults, which can occur 2-6 weeks after SARS-CoV-2 infection. But even in these patients with severe illness, organ-specific complications tend to resolve in 6 months with “no significant sequelae 1 year after diagnosis,” according to the Centers for Disease Control and Prevention. And while long COVID can last for a year or longer, data suggest that symptoms do eventually resolve for most people. What is not clear is why acute autoimmunity triggered by COVID-19 can become a chronic condition in certain patients.
Predisposition to autoimmunity
P. J. Utz, MD, PhD, professor of immunology and rheumatology at Stanford (Calif.) University, said that people who develop autoimmune disease after SARS-CoV-2 infection may have already been predisposed toward autoimmunity. Especially for autoimmune diseases such as type 1 diabetes and lupus, autoantibodies can appear and circulate in the body for more than a decade in some people before they present with any clinical symptoms. “Their immune system is primed such that if they get infected with something – or they have some other environmental trigger that maybe we don’t know about yet – that is enough to then push them over the edge so that they get full-blown autoimmunity,” he said. What is not known is whether these patients’ conditions would have advanced to true clinical disease had they not been infected, he said.
He also noted that the presence of autoantibodies does not necessarily mean someone has autoimmune disease; healthy people can also have autoantibodies, and everyone develops them with age. “My advice would be, ‘Don’t lose sleep over this,’ “ he said.
Dr. Sparks agreed that while these retrospective studies did show an elevated risk of autoimmune disease after COVID-19, that risk appears to be relatively small. “As a practicing rheumatologist, we aren’t seeing a stampede of patients with new-onset rheumatic diseases,” he said. “It’s not like we’re overwhelmed with autoimmune patients, even though almost everyone’s had COVID. So, if there is a risk, it’s very modest.”
Dr. Sparks is supported by the National Institute of Arthritis and Musculoskeletal and Skin Diseases, the R. Bruce and Joan M. Mickey Research Scholar Fund, and the Llura Gund Award for Rheumatoid Arthritis Research and Care. Dr. Utz receives research funding from Pfizer. Dr. Sharma and Dr. Woodruff have disclosed no relevant financial relationships.
A version of this article originally appeared on Medscape.com.
Since the COVID-19 pandemic started more than 3 years ago, the longer-lasting effects of SARS-CoV-2 infection have continued to reveal themselves. Approximately 28% of Americans report having ever experienced post-COVID conditions, such as brain fog, postexertional malaise, and joint pain, and 11% say they are still experiencing these long-term effects. Now, new research is showing that people who have had COVID are more likely to newly develop an autoimmune disease. Exactly why this is happening is less clear, experts say.
Two preprint studies and one study published in a peer-reviewed journal provide strong evidence that patients who have been infected with SARS-CoV-2 are at elevated risk of developing an autoimmune disease. The studies retrospectively reviewed medical records from three countries and compared the incidence of new-onset autoimmune disease among patients who had polymerase chain reaction–confirmed COVID-19 and those who had never been diagnosed with the virus.
A study analyzing the health records of 3.8 million U.S. patients – more than 888,460 with confirmed COVID-19 – found that the COVID-19 group was two to three times as likely to develop various autoimmune diseases, such as rheumatoid arthritis, systemic lupus erythematosus, and systemic sclerosis. A U.K. preprint study that included more than 458,000 people with confirmed COVID found that those who had previously been infected with SARS-CoV-2 were 22% more likely to develop an autoimmune disease compared with the control group. In this cohort, the diseases most strongly associated with COVID-19 were type 1 diabetes, inflammatory bowel disease, and psoriasis. A preprint study from German researchers found that COVID-19 patients were almost 43% more likely to develop an autoimmune disease, compared with those who had never been infected. COVID-19 was most strongly linked to vasculitis.
These large studies are telling us, “Yes, this link is there, so we have to accept it,” Sonia Sharma, PhD, of the Center for Autoimmunity and Inflammation at the La Jolla (Calif.) Institute for Immunology, told this news organization. But this is not the first time that autoimmune diseases have been linked to previous infections.
Researchers have known for decades that Epstein-Barr virus infection is linked to several autoimmune diseases, including systemic lupus erythematosus, multiple sclerosis, and rheumatoid arthritis. More recent research suggests the virus may activate certain genes associated with these immune disorders. Hepatitis C virus can induce cryoglobulinemia, and infection with cytomegalovirus has been implicated in several autoimmune diseases. Bacterial infections have also been linked to autoimmunity, such as group A streptococcus and rheumatic fever, as well as salmonella and reactive arthritis, to name only a few.
“In a way, this isn’t necessarily a new concept to physicians, particularly rheumatologists,” said Jeffrey A. Sparks, MD, a rheumatologist at Brigham and Women’s Hospital in Boston. “There’s a fine line between appropriately clearing an infection and the body overreacting and setting off a cascade where the immune system is chronically overactive that can manifest as an autoimmune disease,” he told this news organization.
A dysregulated response to infection
It takes the immune system a week or two to develop antigen-specific antibodies to a new pathogen. But for patients with serious infections – in this instance, COVID-19 – that’s time they don’t have. Therefore, the immune system has an alternative pathway, called extrafollicular activation, that creates fast-acting antibodies, explained Matthew Woodruff, PhD, an instructor of immunology and rheumatology at Emory University, Atlanta.
The trade-off is that these antibodies are not as specific and can target the body’s own tissues. This dysregulation of antibody selection is generally short lived and fades when more targeted antibodies are produced and take over, but in some cases, this process can lead to high levels of self-targeting antibodies that can harm the body’s organs and tissues. Research also suggests that for patients who experience long COVID, the same autoantibodies that drive the initial immune response are detectable in the body months after infection, though it is not known whether these lingering immune cells cause these longer-lasting symptoms.
“If you have a virus that causes hyperinflammation plus organ damage, that is a recipe for disaster,” Dr. Sharma said. “It’s a recipe for autoantibodies and autoreactive T cells that down the road can attack the body’s own tissues, especially in people whose immune system is trained in such a way to cause self-reactivity,” she added.
This hyperinflammation can result in rare but serious complications, such as multisystem inflammatory syndrome in children and adults, which can occur 2-6 weeks after SARS-CoV-2 infection. But even in these patients with severe illness, organ-specific complications tend to resolve in 6 months with “no significant sequelae 1 year after diagnosis,” according to the Centers for Disease Control and Prevention. And while long COVID can last for a year or longer, data suggest that symptoms do eventually resolve for most people. What is not clear is why acute autoimmunity triggered by COVID-19 can become a chronic condition in certain patients.
Predisposition to autoimmunity
P. J. Utz, MD, PhD, professor of immunology and rheumatology at Stanford (Calif.) University, said that people who develop autoimmune disease after SARS-CoV-2 infection may have already been predisposed toward autoimmunity. Especially for autoimmune diseases such as type 1 diabetes and lupus, autoantibodies can appear and circulate in the body for more than a decade in some people before they present with any clinical symptoms. “Their immune system is primed such that if they get infected with something – or they have some other environmental trigger that maybe we don’t know about yet – that is enough to then push them over the edge so that they get full-blown autoimmunity,” he said. What is not known is whether these patients’ conditions would have advanced to true clinical disease had they not been infected, he said.
He also noted that the presence of autoantibodies does not necessarily mean someone has autoimmune disease; healthy people can also have autoantibodies, and everyone develops them with age. “My advice would be, ‘Don’t lose sleep over this,’ “ he said.
Dr. Sparks agreed that while these retrospective studies did show an elevated risk of autoimmune disease after COVID-19, that risk appears to be relatively small. “As a practicing rheumatologist, we aren’t seeing a stampede of patients with new-onset rheumatic diseases,” he said. “It’s not like we’re overwhelmed with autoimmune patients, even though almost everyone’s had COVID. So, if there is a risk, it’s very modest.”
Dr. Sparks is supported by the National Institute of Arthritis and Musculoskeletal and Skin Diseases, the R. Bruce and Joan M. Mickey Research Scholar Fund, and the Llura Gund Award for Rheumatoid Arthritis Research and Care. Dr. Utz receives research funding from Pfizer. Dr. Sharma and Dr. Woodruff have disclosed no relevant financial relationships.
A version of this article originally appeared on Medscape.com.
Since the COVID-19 pandemic started more than 3 years ago, the longer-lasting effects of SARS-CoV-2 infection have continued to reveal themselves. Approximately 28% of Americans report having ever experienced post-COVID conditions, such as brain fog, postexertional malaise, and joint pain, and 11% say they are still experiencing these long-term effects. Now, new research is showing that people who have had COVID are more likely to newly develop an autoimmune disease. Exactly why this is happening is less clear, experts say.
Two preprint studies and one study published in a peer-reviewed journal provide strong evidence that patients who have been infected with SARS-CoV-2 are at elevated risk of developing an autoimmune disease. The studies retrospectively reviewed medical records from three countries and compared the incidence of new-onset autoimmune disease among patients who had polymerase chain reaction–confirmed COVID-19 and those who had never been diagnosed with the virus.
A study analyzing the health records of 3.8 million U.S. patients – more than 888,460 with confirmed COVID-19 – found that the COVID-19 group was two to three times as likely to develop various autoimmune diseases, such as rheumatoid arthritis, systemic lupus erythematosus, and systemic sclerosis. A U.K. preprint study that included more than 458,000 people with confirmed COVID found that those who had previously been infected with SARS-CoV-2 were 22% more likely to develop an autoimmune disease compared with the control group. In this cohort, the diseases most strongly associated with COVID-19 were type 1 diabetes, inflammatory bowel disease, and psoriasis. A preprint study from German researchers found that COVID-19 patients were almost 43% more likely to develop an autoimmune disease, compared with those who had never been infected. COVID-19 was most strongly linked to vasculitis.
These large studies are telling us, “Yes, this link is there, so we have to accept it,” Sonia Sharma, PhD, of the Center for Autoimmunity and Inflammation at the La Jolla (Calif.) Institute for Immunology, told this news organization. But this is not the first time that autoimmune diseases have been linked to previous infections.
Researchers have known for decades that Epstein-Barr virus infection is linked to several autoimmune diseases, including systemic lupus erythematosus, multiple sclerosis, and rheumatoid arthritis. More recent research suggests the virus may activate certain genes associated with these immune disorders. Hepatitis C virus can induce cryoglobulinemia, and infection with cytomegalovirus has been implicated in several autoimmune diseases. Bacterial infections have also been linked to autoimmunity, such as group A streptococcus and rheumatic fever, as well as salmonella and reactive arthritis, to name only a few.
“In a way, this isn’t necessarily a new concept to physicians, particularly rheumatologists,” said Jeffrey A. Sparks, MD, a rheumatologist at Brigham and Women’s Hospital in Boston. “There’s a fine line between appropriately clearing an infection and the body overreacting and setting off a cascade where the immune system is chronically overactive that can manifest as an autoimmune disease,” he told this news organization.
A dysregulated response to infection
It takes the immune system a week or two to develop antigen-specific antibodies to a new pathogen. But for patients with serious infections – in this instance, COVID-19 – that’s time they don’t have. Therefore, the immune system has an alternative pathway, called extrafollicular activation, that creates fast-acting antibodies, explained Matthew Woodruff, PhD, an instructor of immunology and rheumatology at Emory University, Atlanta.
The trade-off is that these antibodies are not as specific and can target the body’s own tissues. This dysregulation of antibody selection is generally short lived and fades when more targeted antibodies are produced and take over, but in some cases, this process can lead to high levels of self-targeting antibodies that can harm the body’s organs and tissues. Research also suggests that for patients who experience long COVID, the same autoantibodies that drive the initial immune response are detectable in the body months after infection, though it is not known whether these lingering immune cells cause these longer-lasting symptoms.
“If you have a virus that causes hyperinflammation plus organ damage, that is a recipe for disaster,” Dr. Sharma said. “It’s a recipe for autoantibodies and autoreactive T cells that down the road can attack the body’s own tissues, especially in people whose immune system is trained in such a way to cause self-reactivity,” she added.
This hyperinflammation can result in rare but serious complications, such as multisystem inflammatory syndrome in children and adults, which can occur 2-6 weeks after SARS-CoV-2 infection. But even in these patients with severe illness, organ-specific complications tend to resolve in 6 months with “no significant sequelae 1 year after diagnosis,” according to the Centers for Disease Control and Prevention. And while long COVID can last for a year or longer, data suggest that symptoms do eventually resolve for most people. What is not clear is why acute autoimmunity triggered by COVID-19 can become a chronic condition in certain patients.
Predisposition to autoimmunity
P. J. Utz, MD, PhD, professor of immunology and rheumatology at Stanford (Calif.) University, said that people who develop autoimmune disease after SARS-CoV-2 infection may have already been predisposed toward autoimmunity. Especially for autoimmune diseases such as type 1 diabetes and lupus, autoantibodies can appear and circulate in the body for more than a decade in some people before they present with any clinical symptoms. “Their immune system is primed such that if they get infected with something – or they have some other environmental trigger that maybe we don’t know about yet – that is enough to then push them over the edge so that they get full-blown autoimmunity,” he said. What is not known is whether these patients’ conditions would have advanced to true clinical disease had they not been infected, he said.
He also noted that the presence of autoantibodies does not necessarily mean someone has autoimmune disease; healthy people can also have autoantibodies, and everyone develops them with age. “My advice would be, ‘Don’t lose sleep over this,’ “ he said.
Dr. Sparks agreed that while these retrospective studies did show an elevated risk of autoimmune disease after COVID-19, that risk appears to be relatively small. “As a practicing rheumatologist, we aren’t seeing a stampede of patients with new-onset rheumatic diseases,” he said. “It’s not like we’re overwhelmed with autoimmune patients, even though almost everyone’s had COVID. So, if there is a risk, it’s very modest.”
Dr. Sparks is supported by the National Institute of Arthritis and Musculoskeletal and Skin Diseases, the R. Bruce and Joan M. Mickey Research Scholar Fund, and the Llura Gund Award for Rheumatoid Arthritis Research and Care. Dr. Utz receives research funding from Pfizer. Dr. Sharma and Dr. Woodruff have disclosed no relevant financial relationships.
A version of this article originally appeared on Medscape.com.
Long-COVID patients respond differently to COVID vaccines
A new study shows that people with long COVID respond differently to COVID vaccines and that the condition may be caused by a dysfunction of the immune system – possibly explaining why some people experience symptoms for months while others recover and resume normal lives.
The study compared people who already had long COVID with people who had recovered from the virus. Both groups had not yet been vaccinated prior to the study. When researchers analyzed blood samples after people received an initial vaccine dose, they found that people with long COVID and people who had already recovered from the virus had similar immune responses at first. But
The long-COVID group also showed an extra immune response that tried to fight the virus in a secondary way that researchers didn’t expect. Both groups showed an initial increase in their blood of antibodies that primarily target what’s known as the “spike” protein of the coronavirus, which allows the virus to invade healthy cells. But the long-COVID group also showed a prolonged increased immune response that tried to fight the part of the virus related to how it replicates.
“Theoretically, the production of these antibodies could mean that people are more protected from infection,” said researcher Catherine Le, MD, in a statement. “We also need to investigate if the elevated immune response corresponds with severity or number of long–COVID-19 symptoms.”
Dr. Le is codirector of the COVID-19 Recovery Program at Cedars-Sinai Medical Center in Los Angeles, where the study was conducted.
Study participants agreed in September 2020 to participate in long-term COVID research at Cedars-Sinai. The new analysis was published earlier this year in BMC Infectious Diseases and included 245 people who had long COVID and 86 health care workers who had recovered from COVID but did not have long-term symptoms.
For the study, long COVID was defined as having symptoms that lasted more than 12 weeks. Common long-COVID symptoms are fatigue, shortness of breath, and brain dysfunction such as confusion and forgetfulness.
The authors said it’s unclear why the two groups had different immune responses and also noted that their study was limited by a small sample size. Their research of blood samples is ongoing, with the goals of identifying a way to diagnose long COVID with a laboratory test and of better understanding what causes the condition.
A version of this article first appeared on WebMD.com.
A new study shows that people with long COVID respond differently to COVID vaccines and that the condition may be caused by a dysfunction of the immune system – possibly explaining why some people experience symptoms for months while others recover and resume normal lives.
The study compared people who already had long COVID with people who had recovered from the virus. Both groups had not yet been vaccinated prior to the study. When researchers analyzed blood samples after people received an initial vaccine dose, they found that people with long COVID and people who had already recovered from the virus had similar immune responses at first. But
The long-COVID group also showed an extra immune response that tried to fight the virus in a secondary way that researchers didn’t expect. Both groups showed an initial increase in their blood of antibodies that primarily target what’s known as the “spike” protein of the coronavirus, which allows the virus to invade healthy cells. But the long-COVID group also showed a prolonged increased immune response that tried to fight the part of the virus related to how it replicates.
“Theoretically, the production of these antibodies could mean that people are more protected from infection,” said researcher Catherine Le, MD, in a statement. “We also need to investigate if the elevated immune response corresponds with severity or number of long–COVID-19 symptoms.”
Dr. Le is codirector of the COVID-19 Recovery Program at Cedars-Sinai Medical Center in Los Angeles, where the study was conducted.
Study participants agreed in September 2020 to participate in long-term COVID research at Cedars-Sinai. The new analysis was published earlier this year in BMC Infectious Diseases and included 245 people who had long COVID and 86 health care workers who had recovered from COVID but did not have long-term symptoms.
For the study, long COVID was defined as having symptoms that lasted more than 12 weeks. Common long-COVID symptoms are fatigue, shortness of breath, and brain dysfunction such as confusion and forgetfulness.
The authors said it’s unclear why the two groups had different immune responses and also noted that their study was limited by a small sample size. Their research of blood samples is ongoing, with the goals of identifying a way to diagnose long COVID with a laboratory test and of better understanding what causes the condition.
A version of this article first appeared on WebMD.com.
A new study shows that people with long COVID respond differently to COVID vaccines and that the condition may be caused by a dysfunction of the immune system – possibly explaining why some people experience symptoms for months while others recover and resume normal lives.
The study compared people who already had long COVID with people who had recovered from the virus. Both groups had not yet been vaccinated prior to the study. When researchers analyzed blood samples after people received an initial vaccine dose, they found that people with long COVID and people who had already recovered from the virus had similar immune responses at first. But
The long-COVID group also showed an extra immune response that tried to fight the virus in a secondary way that researchers didn’t expect. Both groups showed an initial increase in their blood of antibodies that primarily target what’s known as the “spike” protein of the coronavirus, which allows the virus to invade healthy cells. But the long-COVID group also showed a prolonged increased immune response that tried to fight the part of the virus related to how it replicates.
“Theoretically, the production of these antibodies could mean that people are more protected from infection,” said researcher Catherine Le, MD, in a statement. “We also need to investigate if the elevated immune response corresponds with severity or number of long–COVID-19 symptoms.”
Dr. Le is codirector of the COVID-19 Recovery Program at Cedars-Sinai Medical Center in Los Angeles, where the study was conducted.
Study participants agreed in September 2020 to participate in long-term COVID research at Cedars-Sinai. The new analysis was published earlier this year in BMC Infectious Diseases and included 245 people who had long COVID and 86 health care workers who had recovered from COVID but did not have long-term symptoms.
For the study, long COVID was defined as having symptoms that lasted more than 12 weeks. Common long-COVID symptoms are fatigue, shortness of breath, and brain dysfunction such as confusion and forgetfulness.
The authors said it’s unclear why the two groups had different immune responses and also noted that their study was limited by a small sample size. Their research of blood samples is ongoing, with the goals of identifying a way to diagnose long COVID with a laboratory test and of better understanding what causes the condition.
A version of this article first appeared on WebMD.com.
Diagnosis by dog: Canines detect COVID in schoolchildren with no symptoms
Scent-detecting dogs have long been used to sniff out medical conditions ranging from low blood sugar and cancer to malaria, impending seizures, and migraines – not to mention explosives and narcotics.
Recently, the sensitivity of the canine nose has been tested as a strategy for screening for SARS-CoV-2 infection in schoolchildren showing no outward symptoms of the virus. A pilot study led by Carol A. Glaser, DVM, MD, of the California Department of Public Health in Richmond, found that trained dogs had an accuracy of more than 95% for detecting the odor of volatile organic compounds, or VOCs, produced by COVID-infected individuals.
The authors believe that odor-based diagnosis with dogs could eventually provide a rapid, inexpensive, and noninvasive way to screen large groups for COVID-19 without the need for antigen testing.
“This is a new program with research ongoing, so it would be premature to consider it from a consumer’s perspective,” Dr. Glaser said in an interview. “However, the data look promising and we are hopeful we can continue to pilot various programs in various settings to see where, and if, dogs can be used for biomedical detection.”
In the lab and in the field
In a study published online in JAMA Pediatrics, Dr. Glaser’s group found that after 2 months’ training on COVID-19 scent samples in the laboratory, the dogs detected the presence of the virus more than 95% of the time. Antigen tests were used as a comparative reference.
In medical terms, the dogs achieved a greater than 95% accuracy on two important measures of effectiveness: sensitivity – a test’s ability to correctly detect the positive presence of disease – and specificity – the ability of a test to accurately rule out the presence of disease and identify as negative an uninfected person.
Next, the researchers piloted field tests in 50 visits at 27 schools from April 1 to May 25, 2022, to compare dogs’ detection ability with that of standard laboratory antigen testing. Participants in the completely voluntary screening numbered 1,558 and ranged in age from 9 to 17 years. Of these, 56% were girls and 89% were students. Almost 70% were screened at least twice.
Overall, the field test compared 3,897 paired antigen-vs.-dog screenings. The dogs accurately signaled the presence of 85 infections and ruled out 3,411 infections, for an overall accuracy of 90%. In 383 cases, however, they inaccurately signaled the presence of infection (false positives) and missed 18 actual infections (false negatives). That translated to a sensitivity in the field of 83%, considerably lower than that of their lab performance.
Direct screening of individuals with dogs outside of the lab involved circumstantial factors that likely contributed to decreased sensitivity and specificity, the authors acknowledged. These included such distractions as noise and the presence of excitable young children as well environmental conditions such as wind and other odors. What about dog phobia and dog hair allergy? “Dog screening takes only a few seconds per student and the dogs do not generally touch the participant as they run a line and sniff at ankles,” Dr. Glaser explained.
As for allergies, the rapid, ankle-level screening occurred in outdoor settings. “The chance of allergies is very low. This would be similar to someone who is out walking on the sidewalk and walks by a dog,” Dr. Glaser said.
Last year, a British trial of almost 4,000 adults tested six dogs trained to detect differences in VOCs between COVID-infected and uninfected individuals. Given samples from both groups, the dogs were able to distinguish between infected and uninfected samples with a sensitivity for detecting the virus ranging from 82% to 94% and a specificity for ruling it out of 76% to 92%. And they were able to smell the VOCs even when the viral load was low. The study also tested organic sensors, which proved even more accurate than the canines.
According to lead author James G. Logan, PhD, a disease control expert at the London School of Hygiene & Tropical Medicine in London, “Odour-based diagnostics using dogs and/or sensors may prove a rapid and effective tool for screening large numbers of people. Mathematical modelling suggests that dog screening plus a confirmatory PCR test could detect up to 89% of SARS-CoV-2 infections, averting up to 2.2 times as much transmission compared to isolation of symptomatic individuals only.”
Funding was provided by the Centers for Disease Control and Prevention Foundation (CDCF) to Early Alert Canines for the purchase and care of the dogs and the support of the handlers and trainers. The CDCF had no other role in the study. Coauthor Carol A. Edwards of Early Alert Canines reported receiving grants from the CDCF.
Scent-detecting dogs have long been used to sniff out medical conditions ranging from low blood sugar and cancer to malaria, impending seizures, and migraines – not to mention explosives and narcotics.
Recently, the sensitivity of the canine nose has been tested as a strategy for screening for SARS-CoV-2 infection in schoolchildren showing no outward symptoms of the virus. A pilot study led by Carol A. Glaser, DVM, MD, of the California Department of Public Health in Richmond, found that trained dogs had an accuracy of more than 95% for detecting the odor of volatile organic compounds, or VOCs, produced by COVID-infected individuals.
The authors believe that odor-based diagnosis with dogs could eventually provide a rapid, inexpensive, and noninvasive way to screen large groups for COVID-19 without the need for antigen testing.
“This is a new program with research ongoing, so it would be premature to consider it from a consumer’s perspective,” Dr. Glaser said in an interview. “However, the data look promising and we are hopeful we can continue to pilot various programs in various settings to see where, and if, dogs can be used for biomedical detection.”
In the lab and in the field
In a study published online in JAMA Pediatrics, Dr. Glaser’s group found that after 2 months’ training on COVID-19 scent samples in the laboratory, the dogs detected the presence of the virus more than 95% of the time. Antigen tests were used as a comparative reference.
In medical terms, the dogs achieved a greater than 95% accuracy on two important measures of effectiveness: sensitivity – a test’s ability to correctly detect the positive presence of disease – and specificity – the ability of a test to accurately rule out the presence of disease and identify as negative an uninfected person.
Next, the researchers piloted field tests in 50 visits at 27 schools from April 1 to May 25, 2022, to compare dogs’ detection ability with that of standard laboratory antigen testing. Participants in the completely voluntary screening numbered 1,558 and ranged in age from 9 to 17 years. Of these, 56% were girls and 89% were students. Almost 70% were screened at least twice.
Overall, the field test compared 3,897 paired antigen-vs.-dog screenings. The dogs accurately signaled the presence of 85 infections and ruled out 3,411 infections, for an overall accuracy of 90%. In 383 cases, however, they inaccurately signaled the presence of infection (false positives) and missed 18 actual infections (false negatives). That translated to a sensitivity in the field of 83%, considerably lower than that of their lab performance.
Direct screening of individuals with dogs outside of the lab involved circumstantial factors that likely contributed to decreased sensitivity and specificity, the authors acknowledged. These included such distractions as noise and the presence of excitable young children as well environmental conditions such as wind and other odors. What about dog phobia and dog hair allergy? “Dog screening takes only a few seconds per student and the dogs do not generally touch the participant as they run a line and sniff at ankles,” Dr. Glaser explained.
As for allergies, the rapid, ankle-level screening occurred in outdoor settings. “The chance of allergies is very low. This would be similar to someone who is out walking on the sidewalk and walks by a dog,” Dr. Glaser said.
Last year, a British trial of almost 4,000 adults tested six dogs trained to detect differences in VOCs between COVID-infected and uninfected individuals. Given samples from both groups, the dogs were able to distinguish between infected and uninfected samples with a sensitivity for detecting the virus ranging from 82% to 94% and a specificity for ruling it out of 76% to 92%. And they were able to smell the VOCs even when the viral load was low. The study also tested organic sensors, which proved even more accurate than the canines.
According to lead author James G. Logan, PhD, a disease control expert at the London School of Hygiene & Tropical Medicine in London, “Odour-based diagnostics using dogs and/or sensors may prove a rapid and effective tool for screening large numbers of people. Mathematical modelling suggests that dog screening plus a confirmatory PCR test could detect up to 89% of SARS-CoV-2 infections, averting up to 2.2 times as much transmission compared to isolation of symptomatic individuals only.”
Funding was provided by the Centers for Disease Control and Prevention Foundation (CDCF) to Early Alert Canines for the purchase and care of the dogs and the support of the handlers and trainers. The CDCF had no other role in the study. Coauthor Carol A. Edwards of Early Alert Canines reported receiving grants from the CDCF.
Scent-detecting dogs have long been used to sniff out medical conditions ranging from low blood sugar and cancer to malaria, impending seizures, and migraines – not to mention explosives and narcotics.
Recently, the sensitivity of the canine nose has been tested as a strategy for screening for SARS-CoV-2 infection in schoolchildren showing no outward symptoms of the virus. A pilot study led by Carol A. Glaser, DVM, MD, of the California Department of Public Health in Richmond, found that trained dogs had an accuracy of more than 95% for detecting the odor of volatile organic compounds, or VOCs, produced by COVID-infected individuals.
The authors believe that odor-based diagnosis with dogs could eventually provide a rapid, inexpensive, and noninvasive way to screen large groups for COVID-19 without the need for antigen testing.
“This is a new program with research ongoing, so it would be premature to consider it from a consumer’s perspective,” Dr. Glaser said in an interview. “However, the data look promising and we are hopeful we can continue to pilot various programs in various settings to see where, and if, dogs can be used for biomedical detection.”
In the lab and in the field
In a study published online in JAMA Pediatrics, Dr. Glaser’s group found that after 2 months’ training on COVID-19 scent samples in the laboratory, the dogs detected the presence of the virus more than 95% of the time. Antigen tests were used as a comparative reference.
In medical terms, the dogs achieved a greater than 95% accuracy on two important measures of effectiveness: sensitivity – a test’s ability to correctly detect the positive presence of disease – and specificity – the ability of a test to accurately rule out the presence of disease and identify as negative an uninfected person.
Next, the researchers piloted field tests in 50 visits at 27 schools from April 1 to May 25, 2022, to compare dogs’ detection ability with that of standard laboratory antigen testing. Participants in the completely voluntary screening numbered 1,558 and ranged in age from 9 to 17 years. Of these, 56% were girls and 89% were students. Almost 70% were screened at least twice.
Overall, the field test compared 3,897 paired antigen-vs.-dog screenings. The dogs accurately signaled the presence of 85 infections and ruled out 3,411 infections, for an overall accuracy of 90%. In 383 cases, however, they inaccurately signaled the presence of infection (false positives) and missed 18 actual infections (false negatives). That translated to a sensitivity in the field of 83%, considerably lower than that of their lab performance.
Direct screening of individuals with dogs outside of the lab involved circumstantial factors that likely contributed to decreased sensitivity and specificity, the authors acknowledged. These included such distractions as noise and the presence of excitable young children as well environmental conditions such as wind and other odors. What about dog phobia and dog hair allergy? “Dog screening takes only a few seconds per student and the dogs do not generally touch the participant as they run a line and sniff at ankles,” Dr. Glaser explained.
As for allergies, the rapid, ankle-level screening occurred in outdoor settings. “The chance of allergies is very low. This would be similar to someone who is out walking on the sidewalk and walks by a dog,” Dr. Glaser said.
Last year, a British trial of almost 4,000 adults tested six dogs trained to detect differences in VOCs between COVID-infected and uninfected individuals. Given samples from both groups, the dogs were able to distinguish between infected and uninfected samples with a sensitivity for detecting the virus ranging from 82% to 94% and a specificity for ruling it out of 76% to 92%. And they were able to smell the VOCs even when the viral load was low. The study also tested organic sensors, which proved even more accurate than the canines.
According to lead author James G. Logan, PhD, a disease control expert at the London School of Hygiene & Tropical Medicine in London, “Odour-based diagnostics using dogs and/or sensors may prove a rapid and effective tool for screening large numbers of people. Mathematical modelling suggests that dog screening plus a confirmatory PCR test could detect up to 89% of SARS-CoV-2 infections, averting up to 2.2 times as much transmission compared to isolation of symptomatic individuals only.”
Funding was provided by the Centers for Disease Control and Prevention Foundation (CDCF) to Early Alert Canines for the purchase and care of the dogs and the support of the handlers and trainers. The CDCF had no other role in the study. Coauthor Carol A. Edwards of Early Alert Canines reported receiving grants from the CDCF.
FROM JAMA PEDIATRICS
Explanation proposed for long-COVID symptoms in the CNS
BOSTON – , according to a collaborative study presented at the 2023 annual meeting of the American Academy of Neurology.
Already documented in several other viral infections, such as influenza and human immunodeficiency virus, antigenic imprinting results in production of antibodies to previously encountered viral infections rather than to the immediate threat, according to Marianna Spatola, MD, PhD, a research fellow at the Ragon Institute, Harvard University, Cambridge, Mass.
Original antigenic sin
In the case of persistent neurologic symptoms after COVID, a condition known as neuroPASC (neurological postacute sequelae of SARS-CoV2 infection), antibodies produced for previously encountered coronaviruses rather than for SARS-CoV2 might explain most or all cases, according to the data Dr. Spatola presented.
The evidence for this explanation was drawn from a study of 112 patients evaluated months after an acute episode of COVID-19. Of these, 18 patients had persistent neurologic dysfunction. When compared with the 94 whose infection resolved without sequelae, the patients with prolonged neurologic impairments had relatively low systemic antibody response to SARS-CoV2. However, they showed relatively high antibody responses against other coronaviruses.
This is a pattern consistent with antigenic imprinting, a concept first described more than 60 years ago as original antigenic sin. When the immune system becomes imprinted with an antigen from the first encountered virus from a family of pathogens, it governs all subsequent antibody responses, according to several published studies that have described and evaluated this concept.
Additional evidence
In Dr. Spatola’s study, other differences, particularly in regard to the cerebrospinal fluid (CSF), further supported the role of antigenic imprinting as a cause of neuroPASC. For one, those with elevated immune responses to other common coronaviruses rather than SARS-CoV2 in the CSF relative to the periphery were more likely to have a bad outcome in regard to neurologic symptoms.
Moreover, the CSF in neuroPASC patients “was characterized by increased IgG1 and absence of IgM, suggesting compartmentalized humoral responses within the CSF through selective transfer of antibodies from the serum to the CSF across the blood-brain barrier rather than through intrathecal synthesis,” Dr. Spatola reported.
In the case of COVID-19, the propensity for antigenic imprinting is not difficult to understand.
“The common cold coronaviruses are pretty similar to SARS-CoV2, but they are not exactly the same,” Dr. Spatola said. Her work and studies by others suggest that when antigenic imprinting occurs, “it prevents full maturation of the antibody response.”
NeuroPASC is one of many manifestations of long COVID, but Dr. Spatola pointed out that the immune response in the CSF is unique and the causes of prolonged neurologic impairment after COVID-19 are likely to involve different mechanisms than other long-COVID symptoms.
“Antibodies in the brain are functionally different,” said Dr. Spatola, noting for example that antibody-directed defenses against viral threats show a greater relative reliance on phagocytosis. This might become important in the development of therapeutics for neurologic symptoms of long COVID.
A different phenomenon
The manifestations of neuroPASC are heterogeneous and can include confusion, cognitive dysfunction, headache, encephalitis, and other impairments. Neurologic symptoms occur during acute SARS-CoV2 infections, but neuroPASC appears to be a different phenomenon. These symptoms, which develop after the initial respiratory disease has resolved, were attributed by Dr. Spatola to persistent inflammation that is not necessarily directly related to ongoing infection.
“The reason why some patients develop neuroPASC is unknown, but I think the evidence has pointed to a role for the immune system rather than the virus itself,” Dr. Spatola said.
Currently, neuroPASC is a clinical diagnosis but Dr. Spatola and her coinvestigators are conducting research to identify biomarkers. A viable diagnostic test is not expected imminently. They have identified 150 different features with potential relevance to neuroPASC.
In their comparison of those who did relative to those who did not develop neuroPASC, the initial studies were undertaken 2-4 months after the acute COVID-19 symptoms had resolved. The patients with neuroPASC and those without neurologic sequelae have now been followed for 6-8 months, which Dr. Spatola said was too short to draw firm conclusions about outcomes.
An evolving concept
Despite the small sample size of this study, these are “very interesting data” for considering the pathogenesis of neuroPASC, which is “a concept that is still evolving,” according to Natalia S. Rost, MD, chief of the stroke division, department of neurology, Massachusetts General Hospital, Boston.
Applied to SARS-CoV2, the concept of original antigenic sin “is new” but Dr. Rost said that it might help differentiate neuroPASC from acute neurologic symptoms of COVID-19, which include stroke. She indicated that the work performed by Dr. Spatola and others might eventually explain the pathology while leading to treatment strategies. She cautioned that the concepts explored in this study “need to be further developed” through larger sample sizes and the exploration of other variables that support the hypothesis.
Dr. Spatola and Dr. Rost report no potential conflicts of interest.
BOSTON – , according to a collaborative study presented at the 2023 annual meeting of the American Academy of Neurology.
Already documented in several other viral infections, such as influenza and human immunodeficiency virus, antigenic imprinting results in production of antibodies to previously encountered viral infections rather than to the immediate threat, according to Marianna Spatola, MD, PhD, a research fellow at the Ragon Institute, Harvard University, Cambridge, Mass.
Original antigenic sin
In the case of persistent neurologic symptoms after COVID, a condition known as neuroPASC (neurological postacute sequelae of SARS-CoV2 infection), antibodies produced for previously encountered coronaviruses rather than for SARS-CoV2 might explain most or all cases, according to the data Dr. Spatola presented.
The evidence for this explanation was drawn from a study of 112 patients evaluated months after an acute episode of COVID-19. Of these, 18 patients had persistent neurologic dysfunction. When compared with the 94 whose infection resolved without sequelae, the patients with prolonged neurologic impairments had relatively low systemic antibody response to SARS-CoV2. However, they showed relatively high antibody responses against other coronaviruses.
This is a pattern consistent with antigenic imprinting, a concept first described more than 60 years ago as original antigenic sin. When the immune system becomes imprinted with an antigen from the first encountered virus from a family of pathogens, it governs all subsequent antibody responses, according to several published studies that have described and evaluated this concept.
Additional evidence
In Dr. Spatola’s study, other differences, particularly in regard to the cerebrospinal fluid (CSF), further supported the role of antigenic imprinting as a cause of neuroPASC. For one, those with elevated immune responses to other common coronaviruses rather than SARS-CoV2 in the CSF relative to the periphery were more likely to have a bad outcome in regard to neurologic symptoms.
Moreover, the CSF in neuroPASC patients “was characterized by increased IgG1 and absence of IgM, suggesting compartmentalized humoral responses within the CSF through selective transfer of antibodies from the serum to the CSF across the blood-brain barrier rather than through intrathecal synthesis,” Dr. Spatola reported.
In the case of COVID-19, the propensity for antigenic imprinting is not difficult to understand.
“The common cold coronaviruses are pretty similar to SARS-CoV2, but they are not exactly the same,” Dr. Spatola said. Her work and studies by others suggest that when antigenic imprinting occurs, “it prevents full maturation of the antibody response.”
NeuroPASC is one of many manifestations of long COVID, but Dr. Spatola pointed out that the immune response in the CSF is unique and the causes of prolonged neurologic impairment after COVID-19 are likely to involve different mechanisms than other long-COVID symptoms.
“Antibodies in the brain are functionally different,” said Dr. Spatola, noting for example that antibody-directed defenses against viral threats show a greater relative reliance on phagocytosis. This might become important in the development of therapeutics for neurologic symptoms of long COVID.
A different phenomenon
The manifestations of neuroPASC are heterogeneous and can include confusion, cognitive dysfunction, headache, encephalitis, and other impairments. Neurologic symptoms occur during acute SARS-CoV2 infections, but neuroPASC appears to be a different phenomenon. These symptoms, which develop after the initial respiratory disease has resolved, were attributed by Dr. Spatola to persistent inflammation that is not necessarily directly related to ongoing infection.
“The reason why some patients develop neuroPASC is unknown, but I think the evidence has pointed to a role for the immune system rather than the virus itself,” Dr. Spatola said.
Currently, neuroPASC is a clinical diagnosis but Dr. Spatola and her coinvestigators are conducting research to identify biomarkers. A viable diagnostic test is not expected imminently. They have identified 150 different features with potential relevance to neuroPASC.
In their comparison of those who did relative to those who did not develop neuroPASC, the initial studies were undertaken 2-4 months after the acute COVID-19 symptoms had resolved. The patients with neuroPASC and those without neurologic sequelae have now been followed for 6-8 months, which Dr. Spatola said was too short to draw firm conclusions about outcomes.
An evolving concept
Despite the small sample size of this study, these are “very interesting data” for considering the pathogenesis of neuroPASC, which is “a concept that is still evolving,” according to Natalia S. Rost, MD, chief of the stroke division, department of neurology, Massachusetts General Hospital, Boston.
Applied to SARS-CoV2, the concept of original antigenic sin “is new” but Dr. Rost said that it might help differentiate neuroPASC from acute neurologic symptoms of COVID-19, which include stroke. She indicated that the work performed by Dr. Spatola and others might eventually explain the pathology while leading to treatment strategies. She cautioned that the concepts explored in this study “need to be further developed” through larger sample sizes and the exploration of other variables that support the hypothesis.
Dr. Spatola and Dr. Rost report no potential conflicts of interest.
BOSTON – , according to a collaborative study presented at the 2023 annual meeting of the American Academy of Neurology.
Already documented in several other viral infections, such as influenza and human immunodeficiency virus, antigenic imprinting results in production of antibodies to previously encountered viral infections rather than to the immediate threat, according to Marianna Spatola, MD, PhD, a research fellow at the Ragon Institute, Harvard University, Cambridge, Mass.
Original antigenic sin
In the case of persistent neurologic symptoms after COVID, a condition known as neuroPASC (neurological postacute sequelae of SARS-CoV2 infection), antibodies produced for previously encountered coronaviruses rather than for SARS-CoV2 might explain most or all cases, according to the data Dr. Spatola presented.
The evidence for this explanation was drawn from a study of 112 patients evaluated months after an acute episode of COVID-19. Of these, 18 patients had persistent neurologic dysfunction. When compared with the 94 whose infection resolved without sequelae, the patients with prolonged neurologic impairments had relatively low systemic antibody response to SARS-CoV2. However, they showed relatively high antibody responses against other coronaviruses.
This is a pattern consistent with antigenic imprinting, a concept first described more than 60 years ago as original antigenic sin. When the immune system becomes imprinted with an antigen from the first encountered virus from a family of pathogens, it governs all subsequent antibody responses, according to several published studies that have described and evaluated this concept.
Additional evidence
In Dr. Spatola’s study, other differences, particularly in regard to the cerebrospinal fluid (CSF), further supported the role of antigenic imprinting as a cause of neuroPASC. For one, those with elevated immune responses to other common coronaviruses rather than SARS-CoV2 in the CSF relative to the periphery were more likely to have a bad outcome in regard to neurologic symptoms.
Moreover, the CSF in neuroPASC patients “was characterized by increased IgG1 and absence of IgM, suggesting compartmentalized humoral responses within the CSF through selective transfer of antibodies from the serum to the CSF across the blood-brain barrier rather than through intrathecal synthesis,” Dr. Spatola reported.
In the case of COVID-19, the propensity for antigenic imprinting is not difficult to understand.
“The common cold coronaviruses are pretty similar to SARS-CoV2, but they are not exactly the same,” Dr. Spatola said. Her work and studies by others suggest that when antigenic imprinting occurs, “it prevents full maturation of the antibody response.”
NeuroPASC is one of many manifestations of long COVID, but Dr. Spatola pointed out that the immune response in the CSF is unique and the causes of prolonged neurologic impairment after COVID-19 are likely to involve different mechanisms than other long-COVID symptoms.
“Antibodies in the brain are functionally different,” said Dr. Spatola, noting for example that antibody-directed defenses against viral threats show a greater relative reliance on phagocytosis. This might become important in the development of therapeutics for neurologic symptoms of long COVID.
A different phenomenon
The manifestations of neuroPASC are heterogeneous and can include confusion, cognitive dysfunction, headache, encephalitis, and other impairments. Neurologic symptoms occur during acute SARS-CoV2 infections, but neuroPASC appears to be a different phenomenon. These symptoms, which develop after the initial respiratory disease has resolved, were attributed by Dr. Spatola to persistent inflammation that is not necessarily directly related to ongoing infection.
“The reason why some patients develop neuroPASC is unknown, but I think the evidence has pointed to a role for the immune system rather than the virus itself,” Dr. Spatola said.
Currently, neuroPASC is a clinical diagnosis but Dr. Spatola and her coinvestigators are conducting research to identify biomarkers. A viable diagnostic test is not expected imminently. They have identified 150 different features with potential relevance to neuroPASC.
In their comparison of those who did relative to those who did not develop neuroPASC, the initial studies were undertaken 2-4 months after the acute COVID-19 symptoms had resolved. The patients with neuroPASC and those without neurologic sequelae have now been followed for 6-8 months, which Dr. Spatola said was too short to draw firm conclusions about outcomes.
An evolving concept
Despite the small sample size of this study, these are “very interesting data” for considering the pathogenesis of neuroPASC, which is “a concept that is still evolving,” according to Natalia S. Rost, MD, chief of the stroke division, department of neurology, Massachusetts General Hospital, Boston.
Applied to SARS-CoV2, the concept of original antigenic sin “is new” but Dr. Rost said that it might help differentiate neuroPASC from acute neurologic symptoms of COVID-19, which include stroke. She indicated that the work performed by Dr. Spatola and others might eventually explain the pathology while leading to treatment strategies. She cautioned that the concepts explored in this study “need to be further developed” through larger sample sizes and the exploration of other variables that support the hypothesis.
Dr. Spatola and Dr. Rost report no potential conflicts of interest.
FROM AAN 2023
CDC backs FDA’s call for second COVID booster for those at high risk
This backs the Food and Drug Administration’s authorization April 18 of the additional shot.
“Following FDA regulatory action, CDC has taken steps to simplify COVID-19 vaccine recommendations and allow more flexibility for people at higher risk who want the option of added protection from additional COVID-19 vaccine doses,” the CDC said in a statement.
The agency is following the recommendations made by its Advisory Committee on Immunization Practices (ACIP). While there was no vote, the group reaffirmed its commitment to boosters overall, proposing that all Americans over age 6 who have not had a bivalent mRNA COVID-19 booster vaccine go ahead and get one.
But most others who’ve already had the bivalent shot – which targets the original COVID strain and the two Omicron variants BA.4 and BA.5 – should wait until the fall to get whatever updated vaccine is available.
The panel did carve out exceptions for people over age 65 and those who are immunocompromised because they are at higher risk for severe COVID-19 complications, Evelyn Twentyman, MD, MPH, the lead official in the CDC’s COVID-19 Vaccine Policy Unit, said during the meeting.
People over 65 can now choose to get a second bivalent mRNA booster shot as long as it has been at least 4 months since the last one, she said, and people who are immunocompromised also should have the flexibility to receive one or more additional bivalent boosters at least 2 months after an initial dose.
Regardless of whether someone is unvaccinated, and regardless of how many single-strain COVID vaccines an individual has previously received, they should get a mRNA bivalent shot, Dr. Twentyman said.
If an individual has already received a bivalent mRNA booster – made by either Pfizer/BioNTech or Moderna – “your vaccination is complete,” she said. “No doses indicated at this time, come back and see us in autumn of 2023.”
The CDC is trying to encourage more people to get the updated COVID shot, as just 17% of Americans of any age have received a bivalent booster and only 43% of those age 65 and over.
The CDC followed the FDA’s lead in its statement, phasing out the original single-strain COVID vaccine, saying it will no longer be recommended for use in the United States.
‘Unnecessary drama’ over children’s recs
The CDC panel mostly followed the FDA’s guidance on who should get a booster, but many ACIP members expressed consternation and confusion about what was being recommended for children.
For children aged 6 months to 4 years, the CDC will offer tables to help physicians determine how many bivalent doses to give, depending on the child’s vaccination history.
All children those ages should get at least two vaccine doses, one of which is bivalent, Dr. Twentyman said. For children in that age group who have already received a monovalent series and a bivalent dose, “their vaccination is complete,” she said.
For 5-year-olds, the recommendations will be similar if they received a Pfizer monovalent series, but the shot regimen will have to be customized if they had previously received a Moderna shot, because of differences in the dosages.
ACIP member Sarah S. Long, MD, professor of pediatrics, Drexel University, Philadelphia, said that it was unclear why a set age couldn’t be established for COVID-19 vaccination as it had been for other immunizations.
“We picked 60 months for most immunizations in children,” Dr. Long said. “Immunologically there is not a difference between a 4-, a 5- and a 6-year-old.
“There isn’t a reason to have all this unnecessary drama around those ages,” she said, adding that having the different ages would make it harder for pediatricians to appropriately stock vaccines.
Dr. Twentyman said that the CDC would be providing more detailed guidance on its COVID-19 website soon and would be holding a call with health care professionals to discuss the updated recommendations on May 11.
New vaccine by fall
CDC and ACIP members both said they hoped to have an even simpler vaccine schedule by the fall, when it is anticipated that the FDA may have authorized a new, updated bivalent vaccine that targets other COVID variants.
“We all recognize this is a work in progress,” said ACIP Chair Grace M. Lee, MD, MPH, acknowledging that there is continued confusion over COVID-19 vaccination.
“The goal really is to try to simplify things over time to be able to help communicate with our provider community, and our patients and families what vaccine is right for them, when do they need it, and how often should they get it,” said Dr. Lee, professor of pediatrics, Stanford (Calif.) University.
A version of this article originally appeared on Medscape.com .
This backs the Food and Drug Administration’s authorization April 18 of the additional shot.
“Following FDA regulatory action, CDC has taken steps to simplify COVID-19 vaccine recommendations and allow more flexibility for people at higher risk who want the option of added protection from additional COVID-19 vaccine doses,” the CDC said in a statement.
The agency is following the recommendations made by its Advisory Committee on Immunization Practices (ACIP). While there was no vote, the group reaffirmed its commitment to boosters overall, proposing that all Americans over age 6 who have not had a bivalent mRNA COVID-19 booster vaccine go ahead and get one.
But most others who’ve already had the bivalent shot – which targets the original COVID strain and the two Omicron variants BA.4 and BA.5 – should wait until the fall to get whatever updated vaccine is available.
The panel did carve out exceptions for people over age 65 and those who are immunocompromised because they are at higher risk for severe COVID-19 complications, Evelyn Twentyman, MD, MPH, the lead official in the CDC’s COVID-19 Vaccine Policy Unit, said during the meeting.
People over 65 can now choose to get a second bivalent mRNA booster shot as long as it has been at least 4 months since the last one, she said, and people who are immunocompromised also should have the flexibility to receive one or more additional bivalent boosters at least 2 months after an initial dose.
Regardless of whether someone is unvaccinated, and regardless of how many single-strain COVID vaccines an individual has previously received, they should get a mRNA bivalent shot, Dr. Twentyman said.
If an individual has already received a bivalent mRNA booster – made by either Pfizer/BioNTech or Moderna – “your vaccination is complete,” she said. “No doses indicated at this time, come back and see us in autumn of 2023.”
The CDC is trying to encourage more people to get the updated COVID shot, as just 17% of Americans of any age have received a bivalent booster and only 43% of those age 65 and over.
The CDC followed the FDA’s lead in its statement, phasing out the original single-strain COVID vaccine, saying it will no longer be recommended for use in the United States.
‘Unnecessary drama’ over children’s recs
The CDC panel mostly followed the FDA’s guidance on who should get a booster, but many ACIP members expressed consternation and confusion about what was being recommended for children.
For children aged 6 months to 4 years, the CDC will offer tables to help physicians determine how many bivalent doses to give, depending on the child’s vaccination history.
All children those ages should get at least two vaccine doses, one of which is bivalent, Dr. Twentyman said. For children in that age group who have already received a monovalent series and a bivalent dose, “their vaccination is complete,” she said.
For 5-year-olds, the recommendations will be similar if they received a Pfizer monovalent series, but the shot regimen will have to be customized if they had previously received a Moderna shot, because of differences in the dosages.
ACIP member Sarah S. Long, MD, professor of pediatrics, Drexel University, Philadelphia, said that it was unclear why a set age couldn’t be established for COVID-19 vaccination as it had been for other immunizations.
“We picked 60 months for most immunizations in children,” Dr. Long said. “Immunologically there is not a difference between a 4-, a 5- and a 6-year-old.
“There isn’t a reason to have all this unnecessary drama around those ages,” she said, adding that having the different ages would make it harder for pediatricians to appropriately stock vaccines.
Dr. Twentyman said that the CDC would be providing more detailed guidance on its COVID-19 website soon and would be holding a call with health care professionals to discuss the updated recommendations on May 11.
New vaccine by fall
CDC and ACIP members both said they hoped to have an even simpler vaccine schedule by the fall, when it is anticipated that the FDA may have authorized a new, updated bivalent vaccine that targets other COVID variants.
“We all recognize this is a work in progress,” said ACIP Chair Grace M. Lee, MD, MPH, acknowledging that there is continued confusion over COVID-19 vaccination.
“The goal really is to try to simplify things over time to be able to help communicate with our provider community, and our patients and families what vaccine is right for them, when do they need it, and how often should they get it,” said Dr. Lee, professor of pediatrics, Stanford (Calif.) University.
A version of this article originally appeared on Medscape.com .
This backs the Food and Drug Administration’s authorization April 18 of the additional shot.
“Following FDA regulatory action, CDC has taken steps to simplify COVID-19 vaccine recommendations and allow more flexibility for people at higher risk who want the option of added protection from additional COVID-19 vaccine doses,” the CDC said in a statement.
The agency is following the recommendations made by its Advisory Committee on Immunization Practices (ACIP). While there was no vote, the group reaffirmed its commitment to boosters overall, proposing that all Americans over age 6 who have not had a bivalent mRNA COVID-19 booster vaccine go ahead and get one.
But most others who’ve already had the bivalent shot – which targets the original COVID strain and the two Omicron variants BA.4 and BA.5 – should wait until the fall to get whatever updated vaccine is available.
The panel did carve out exceptions for people over age 65 and those who are immunocompromised because they are at higher risk for severe COVID-19 complications, Evelyn Twentyman, MD, MPH, the lead official in the CDC’s COVID-19 Vaccine Policy Unit, said during the meeting.
People over 65 can now choose to get a second bivalent mRNA booster shot as long as it has been at least 4 months since the last one, she said, and people who are immunocompromised also should have the flexibility to receive one or more additional bivalent boosters at least 2 months after an initial dose.
Regardless of whether someone is unvaccinated, and regardless of how many single-strain COVID vaccines an individual has previously received, they should get a mRNA bivalent shot, Dr. Twentyman said.
If an individual has already received a bivalent mRNA booster – made by either Pfizer/BioNTech or Moderna – “your vaccination is complete,” she said. “No doses indicated at this time, come back and see us in autumn of 2023.”
The CDC is trying to encourage more people to get the updated COVID shot, as just 17% of Americans of any age have received a bivalent booster and only 43% of those age 65 and over.
The CDC followed the FDA’s lead in its statement, phasing out the original single-strain COVID vaccine, saying it will no longer be recommended for use in the United States.
‘Unnecessary drama’ over children’s recs
The CDC panel mostly followed the FDA’s guidance on who should get a booster, but many ACIP members expressed consternation and confusion about what was being recommended for children.
For children aged 6 months to 4 years, the CDC will offer tables to help physicians determine how many bivalent doses to give, depending on the child’s vaccination history.
All children those ages should get at least two vaccine doses, one of which is bivalent, Dr. Twentyman said. For children in that age group who have already received a monovalent series and a bivalent dose, “their vaccination is complete,” she said.
For 5-year-olds, the recommendations will be similar if they received a Pfizer monovalent series, but the shot regimen will have to be customized if they had previously received a Moderna shot, because of differences in the dosages.
ACIP member Sarah S. Long, MD, professor of pediatrics, Drexel University, Philadelphia, said that it was unclear why a set age couldn’t be established for COVID-19 vaccination as it had been for other immunizations.
“We picked 60 months for most immunizations in children,” Dr. Long said. “Immunologically there is not a difference between a 4-, a 5- and a 6-year-old.
“There isn’t a reason to have all this unnecessary drama around those ages,” she said, adding that having the different ages would make it harder for pediatricians to appropriately stock vaccines.
Dr. Twentyman said that the CDC would be providing more detailed guidance on its COVID-19 website soon and would be holding a call with health care professionals to discuss the updated recommendations on May 11.
New vaccine by fall
CDC and ACIP members both said they hoped to have an even simpler vaccine schedule by the fall, when it is anticipated that the FDA may have authorized a new, updated bivalent vaccine that targets other COVID variants.
“We all recognize this is a work in progress,” said ACIP Chair Grace M. Lee, MD, MPH, acknowledging that there is continued confusion over COVID-19 vaccination.
“The goal really is to try to simplify things over time to be able to help communicate with our provider community, and our patients and families what vaccine is right for them, when do they need it, and how often should they get it,” said Dr. Lee, professor of pediatrics, Stanford (Calif.) University.
A version of this article originally appeared on Medscape.com .
New variant jumps to second place on COVID list
Officially labeled XBB.1.16, Arcturus is a subvariant of Omicron that was first seen in India and has been on the World Health Organization’s watchlist since the end of March. The CDC’s most recent update now lists Arcturus as causing 7% of U.S. coronavirus cases, landing it in second place behind its long-predominant Omicron cousin XBB.1.5, which causes 78% of cases.
Arcturus is more transmissible but not more dangerous than recent chart-topping strains, experts say.
“It is causing increasing case counts in certain parts of the world, including India. We’re not seeing high rates of XBB.1.16 yet in the United States, but it may become more prominent in coming weeks,” Mayo Clinic viral disease expert Matthew Binnicker, PhD, told The Seattle Times.
Arcturus has been causing a new symptom in children, Indian medical providers have reported.
“One new feature of cases caused by this variant is that it seems to be causing conjunctivitis, or red and itchy eyes, in young patients,” Dr. Binnicker said. “This is not something that we’ve seen with prior strains of the virus.”
More than 11,000 people in the United States remained hospitalized with COVID at the end of last week, and 1,327 people died of the virus last week, CDC data show. To date, 6.9 million people worldwide have died from COVID, the WHO says. Of those deaths, more than 1.1 million occurred in the U.S.
A version of this article originally appeared on WebMD.com.
Officially labeled XBB.1.16, Arcturus is a subvariant of Omicron that was first seen in India and has been on the World Health Organization’s watchlist since the end of March. The CDC’s most recent update now lists Arcturus as causing 7% of U.S. coronavirus cases, landing it in second place behind its long-predominant Omicron cousin XBB.1.5, which causes 78% of cases.
Arcturus is more transmissible but not more dangerous than recent chart-topping strains, experts say.
“It is causing increasing case counts in certain parts of the world, including India. We’re not seeing high rates of XBB.1.16 yet in the United States, but it may become more prominent in coming weeks,” Mayo Clinic viral disease expert Matthew Binnicker, PhD, told The Seattle Times.
Arcturus has been causing a new symptom in children, Indian medical providers have reported.
“One new feature of cases caused by this variant is that it seems to be causing conjunctivitis, or red and itchy eyes, in young patients,” Dr. Binnicker said. “This is not something that we’ve seen with prior strains of the virus.”
More than 11,000 people in the United States remained hospitalized with COVID at the end of last week, and 1,327 people died of the virus last week, CDC data show. To date, 6.9 million people worldwide have died from COVID, the WHO says. Of those deaths, more than 1.1 million occurred in the U.S.
A version of this article originally appeared on WebMD.com.
Officially labeled XBB.1.16, Arcturus is a subvariant of Omicron that was first seen in India and has been on the World Health Organization’s watchlist since the end of March. The CDC’s most recent update now lists Arcturus as causing 7% of U.S. coronavirus cases, landing it in second place behind its long-predominant Omicron cousin XBB.1.5, which causes 78% of cases.
Arcturus is more transmissible but not more dangerous than recent chart-topping strains, experts say.
“It is causing increasing case counts in certain parts of the world, including India. We’re not seeing high rates of XBB.1.16 yet in the United States, but it may become more prominent in coming weeks,” Mayo Clinic viral disease expert Matthew Binnicker, PhD, told The Seattle Times.
Arcturus has been causing a new symptom in children, Indian medical providers have reported.
“One new feature of cases caused by this variant is that it seems to be causing conjunctivitis, or red and itchy eyes, in young patients,” Dr. Binnicker said. “This is not something that we’ve seen with prior strains of the virus.”
More than 11,000 people in the United States remained hospitalized with COVID at the end of last week, and 1,327 people died of the virus last week, CDC data show. To date, 6.9 million people worldwide have died from COVID, the WHO says. Of those deaths, more than 1.1 million occurred in the U.S.
A version of this article originally appeared on WebMD.com.
As COVID tracking wanes, are we letting our guard down too soon?
The 30-second commercial, part of the government’s We Can Do This campaign, shows everyday people going about their lives, then reminds them that, “because COVID is still out there and so are you,” it might be time to update your vaccine.
Many data tracking sources, both federal and others, are no longer reporting, as often, the number of COVID cases, hospitalizations, and deaths.
The Department of Health & Human Services in February stopped updating its public COVID data site, instead directing all queries to the Centers for Disease Control and Prevention, which itself has been updating only weekly instead of daily since 2022.
Nongovernmental sources, such as John Hopkins University, stopped reporting pandemic data in March, The New York Times also ended its COVID data-gathering project in March, stating that “the comprehensive real-time reporting that The Times has prioritized is no longer possible.” It will rely on reporting weekly CDC data moving forward.
Along with the tracking sites, masking and social distancing mandates have mostly disappeared. President Joe Biden signed a bipartisan bill on April 10 that ended the national emergency for COVID. While some programs will stay in place for now, such as free vaccines, treatments, and tests, that too will go away when the federal public health emergency expires on May 11. The HHS already has issued its transition roadmap.
Many Americans, meanwhile, are still on the fence about the pandemic. A Gallup poll from March shows that about half of the American public say it’s over, and about half disagree.
Are we closing up shop on COVID-19 too soon, or is it time? Not surprisingly, experts don’t agree. Some say the pandemic is now endemic – which broadly means the virus and its patterns are predictable and steady in designated regions – and that it’s critical to catch up on health needs neglected during the pandemic, such as screenings and other vaccinations
But others don’t think it’s reached that stage yet, saying that we are letting our guard down too soon and we can’t be blind to the possibility of another strong variant – or pandemic – emerging. Surveillance must continue, not decline, and be improved.
Time to move on?
In its transition roadmap released in February, the HHS notes that daily COVID reported cases are down over 90%, compared with the peak of the Omicron surge at the end of January 2022; deaths have declined by over 80%; and new hospitalizations caused by COVID have dropped by nearly 80%.
It is time to move on, said Ali Mokdad, PhD, a professor and chief strategy officer of population health at the Institute for Health Metrics and Evaluation at the University of Washington, Seattle.
“Many people were delaying a lot of medical care, because they were afraid” during COVID’s height, he said, explaining that elective surgeries were postponed, prenatal care went down, as did screenings for blood pressure and diabetes.
His institute was tracking COVID projections every week but stopped in December.
As for emerging variants, “we haven’t seen a variant that scares us since Omicron” in November 2021, said Dr. Mokdad, who agrees that COVID is endemic now. The subvariants that followed it are very similar, and the current vaccines are working.
“We can move on, but we cannot drop the ball on keeping an eye on the genetic sequencing of the virus,” he said. That will enable quick identification of new variants.
If a worrisome new variant does surface, Dr. Mokdad said, certain locations and resources will be able to gear up quickly, while others won’t be as fast, but overall the United States is in a much better position now.
Amesh Adalja, MD, a senior scholar at the Johns Hopkins Center for Health Security, Baltimore, also believes the pandemic phase is behind us
“This can’t be an emergency in perpetuity,” he said “Just because something is not a pandemic [anymore] does not mean that all activities related to it cease.”
COVID is highly unlikely to overwhelm hospitals again, and that was the main reason for the emergency declaration, he said.
“It’s not all or none – collapsing COVID-related [monitoring] activities into the routine monitoring that is done for other infectious disease should be seen as an achievement in taming the virus,” he said.
Not endemic yet
Closing up shop too early could mean we are blindsided, said Rajendram Rajnarayanan, PhD, an assistant dean of research and associate professor at the New York Institute of Technology College of Osteopathic Medicine at Arkansas State University in Jonesboro.
Already, he said, large labs have closed or scaled down as testing demand has declined, and many centers that offered community testing have also closed. Plus, home test results are often not reported.
Continued monitoring is key, he said. “You have to maintain a base level of sequencing for new variants,” he said. “Right now, the variant that is ‘top dog’ in the world is XBB.1.16.”
That’s an Omicron subvariant that the World Health Organization is currently keeping its eye on, according to a media briefing on March 29. There are about 800 sequences of it from 22 countries, mostly India, and it’s been in circulation a few months.
Dr. Rajnarayanan said he’s not overly worried about this variant, but surveillance must continue. His own breakdown of XBB.1.16 found the subvariant in 27 countries, including the United States, as of April 10.
Ideally, Dr. Rajnarayanan would suggest four areas to keep focusing on, moving forward:
- Active, random surveillance for new variants, especially in hot spots.
- Hospital surveillance and surveillance of long-term care, especially in congregate settings where people can more easily spread the virus.
- Travelers’ surveillance, now at , according to the CDC.
- Surveillance of animals such as mink and deer, because these animals can not only pick up the virus, but the virus can mutate in the animals, which could then transmit it back to people.
With less testing, baseline surveillance for new variants has declined. The other three surveillance areas need improvement, too, he said, as the reporting is often delayed.
Continued surveillance is crucial, agreed Katelyn Jetelina, PhD, an epidemiologist and data scientist who publishes a newsletter, Your Local Epidemiologist, updating developments in COVID and other pressing health issues.
“It’s a bit ironic to have a date for the end of a public health emergency; viruses don’t care about calendars,” said Dr. Jetelina, who is also director of population health analytics for the Meadows Mental Health Policy Institute. “COVID-19 is still going to be here, it’s still going to mutate,” and still cause grief for those affected. “I’m most concerned about our ability to track the virus. It’s not clear what surveillance we will still have in the states and around the globe.”
It’s a bit ironic to have a date for the end of a public health emergency; viruses don’t care about calendars.
For surveillance, she calls wastewater monitoring “the lowest-hanging fruit.” That’s because it “is not based on bias testing and has the potential to help with other outbreaks, too.” Hospitalization data is also essential, she said, as that information is the basis for public health decisions on updated vaccines and other protective measures.
While Dr. Jetelina is hopeful that COVID will someday be universally viewed as endemic, with predictable seasonal patterns, “I don’t think we are there yet. We still need to approach this virus with humility; that’s at least what I will continue to do.”
Dr. Rajnarayanan agreed that the pandemic has not yet reached endemic phase, though the situation is much improved. “Our vaccines are still protecting us from severe disease and hospitalization, and [the antiviral drug] Paxlovid is a great tool that works.”
Keeping tabs
While some data tracking has been eliminated, not all has, or will be. The CDC, as mentioned, continues to post cases, deaths, and a daily average of new hospital admissions weekly. The WHO’s dashboard tracks deaths, cases, and vaccine doses globally.
In March, the WHO updated its working definitions and tracking system for SARS-CoV-2 variants of concern and variants of interest, with goals of evaluating the sublineages independently and to classify new variants more clearly when that’s needed.
Still, WHO is considering ending its declaration of COVID as a public health emergency of international concern sometime in 2023.
Some public companies are staying vigilant. The drugstore chain Walgreens said it plans to maintain its COVID-19 Index, which launched in January 2022.
“Data regarding spread of variants is important to our understanding of viral transmission and, as new variants emerge, it will be critical to continue to track this information quickly to predict which communities are most at risk,” Anita Patel, PharmD, vice president of pharmacy services development for Walgreens, said in a statement.
The data also reinforces the importance of vaccinations and testing in helping to stop the spread of COVID-19, she said.
A version of this article first appeared on WebMD.com.
The 30-second commercial, part of the government’s We Can Do This campaign, shows everyday people going about their lives, then reminds them that, “because COVID is still out there and so are you,” it might be time to update your vaccine.
Many data tracking sources, both federal and others, are no longer reporting, as often, the number of COVID cases, hospitalizations, and deaths.
The Department of Health & Human Services in February stopped updating its public COVID data site, instead directing all queries to the Centers for Disease Control and Prevention, which itself has been updating only weekly instead of daily since 2022.
Nongovernmental sources, such as John Hopkins University, stopped reporting pandemic data in March, The New York Times also ended its COVID data-gathering project in March, stating that “the comprehensive real-time reporting that The Times has prioritized is no longer possible.” It will rely on reporting weekly CDC data moving forward.
Along with the tracking sites, masking and social distancing mandates have mostly disappeared. President Joe Biden signed a bipartisan bill on April 10 that ended the national emergency for COVID. While some programs will stay in place for now, such as free vaccines, treatments, and tests, that too will go away when the federal public health emergency expires on May 11. The HHS already has issued its transition roadmap.
Many Americans, meanwhile, are still on the fence about the pandemic. A Gallup poll from March shows that about half of the American public say it’s over, and about half disagree.
Are we closing up shop on COVID-19 too soon, or is it time? Not surprisingly, experts don’t agree. Some say the pandemic is now endemic – which broadly means the virus and its patterns are predictable and steady in designated regions – and that it’s critical to catch up on health needs neglected during the pandemic, such as screenings and other vaccinations
But others don’t think it’s reached that stage yet, saying that we are letting our guard down too soon and we can’t be blind to the possibility of another strong variant – or pandemic – emerging. Surveillance must continue, not decline, and be improved.
Time to move on?
In its transition roadmap released in February, the HHS notes that daily COVID reported cases are down over 90%, compared with the peak of the Omicron surge at the end of January 2022; deaths have declined by over 80%; and new hospitalizations caused by COVID have dropped by nearly 80%.
It is time to move on, said Ali Mokdad, PhD, a professor and chief strategy officer of population health at the Institute for Health Metrics and Evaluation at the University of Washington, Seattle.
“Many people were delaying a lot of medical care, because they were afraid” during COVID’s height, he said, explaining that elective surgeries were postponed, prenatal care went down, as did screenings for blood pressure and diabetes.
His institute was tracking COVID projections every week but stopped in December.
As for emerging variants, “we haven’t seen a variant that scares us since Omicron” in November 2021, said Dr. Mokdad, who agrees that COVID is endemic now. The subvariants that followed it are very similar, and the current vaccines are working.
“We can move on, but we cannot drop the ball on keeping an eye on the genetic sequencing of the virus,” he said. That will enable quick identification of new variants.
If a worrisome new variant does surface, Dr. Mokdad said, certain locations and resources will be able to gear up quickly, while others won’t be as fast, but overall the United States is in a much better position now.
Amesh Adalja, MD, a senior scholar at the Johns Hopkins Center for Health Security, Baltimore, also believes the pandemic phase is behind us
“This can’t be an emergency in perpetuity,” he said “Just because something is not a pandemic [anymore] does not mean that all activities related to it cease.”
COVID is highly unlikely to overwhelm hospitals again, and that was the main reason for the emergency declaration, he said.
“It’s not all or none – collapsing COVID-related [monitoring] activities into the routine monitoring that is done for other infectious disease should be seen as an achievement in taming the virus,” he said.
Not endemic yet
Closing up shop too early could mean we are blindsided, said Rajendram Rajnarayanan, PhD, an assistant dean of research and associate professor at the New York Institute of Technology College of Osteopathic Medicine at Arkansas State University in Jonesboro.
Already, he said, large labs have closed or scaled down as testing demand has declined, and many centers that offered community testing have also closed. Plus, home test results are often not reported.
Continued monitoring is key, he said. “You have to maintain a base level of sequencing for new variants,” he said. “Right now, the variant that is ‘top dog’ in the world is XBB.1.16.”
That’s an Omicron subvariant that the World Health Organization is currently keeping its eye on, according to a media briefing on March 29. There are about 800 sequences of it from 22 countries, mostly India, and it’s been in circulation a few months.
Dr. Rajnarayanan said he’s not overly worried about this variant, but surveillance must continue. His own breakdown of XBB.1.16 found the subvariant in 27 countries, including the United States, as of April 10.
Ideally, Dr. Rajnarayanan would suggest four areas to keep focusing on, moving forward:
- Active, random surveillance for new variants, especially in hot spots.
- Hospital surveillance and surveillance of long-term care, especially in congregate settings where people can more easily spread the virus.
- Travelers’ surveillance, now at , according to the CDC.
- Surveillance of animals such as mink and deer, because these animals can not only pick up the virus, but the virus can mutate in the animals, which could then transmit it back to people.
With less testing, baseline surveillance for new variants has declined. The other three surveillance areas need improvement, too, he said, as the reporting is often delayed.
Continued surveillance is crucial, agreed Katelyn Jetelina, PhD, an epidemiologist and data scientist who publishes a newsletter, Your Local Epidemiologist, updating developments in COVID and other pressing health issues.
“It’s a bit ironic to have a date for the end of a public health emergency; viruses don’t care about calendars,” said Dr. Jetelina, who is also director of population health analytics for the Meadows Mental Health Policy Institute. “COVID-19 is still going to be here, it’s still going to mutate,” and still cause grief for those affected. “I’m most concerned about our ability to track the virus. It’s not clear what surveillance we will still have in the states and around the globe.”
It’s a bit ironic to have a date for the end of a public health emergency; viruses don’t care about calendars.
For surveillance, she calls wastewater monitoring “the lowest-hanging fruit.” That’s because it “is not based on bias testing and has the potential to help with other outbreaks, too.” Hospitalization data is also essential, she said, as that information is the basis for public health decisions on updated vaccines and other protective measures.
While Dr. Jetelina is hopeful that COVID will someday be universally viewed as endemic, with predictable seasonal patterns, “I don’t think we are there yet. We still need to approach this virus with humility; that’s at least what I will continue to do.”
Dr. Rajnarayanan agreed that the pandemic has not yet reached endemic phase, though the situation is much improved. “Our vaccines are still protecting us from severe disease and hospitalization, and [the antiviral drug] Paxlovid is a great tool that works.”
Keeping tabs
While some data tracking has been eliminated, not all has, or will be. The CDC, as mentioned, continues to post cases, deaths, and a daily average of new hospital admissions weekly. The WHO’s dashboard tracks deaths, cases, and vaccine doses globally.
In March, the WHO updated its working definitions and tracking system for SARS-CoV-2 variants of concern and variants of interest, with goals of evaluating the sublineages independently and to classify new variants more clearly when that’s needed.
Still, WHO is considering ending its declaration of COVID as a public health emergency of international concern sometime in 2023.
Some public companies are staying vigilant. The drugstore chain Walgreens said it plans to maintain its COVID-19 Index, which launched in January 2022.
“Data regarding spread of variants is important to our understanding of viral transmission and, as new variants emerge, it will be critical to continue to track this information quickly to predict which communities are most at risk,” Anita Patel, PharmD, vice president of pharmacy services development for Walgreens, said in a statement.
The data also reinforces the importance of vaccinations and testing in helping to stop the spread of COVID-19, she said.
A version of this article first appeared on WebMD.com.
The 30-second commercial, part of the government’s We Can Do This campaign, shows everyday people going about their lives, then reminds them that, “because COVID is still out there and so are you,” it might be time to update your vaccine.
Many data tracking sources, both federal and others, are no longer reporting, as often, the number of COVID cases, hospitalizations, and deaths.
The Department of Health & Human Services in February stopped updating its public COVID data site, instead directing all queries to the Centers for Disease Control and Prevention, which itself has been updating only weekly instead of daily since 2022.
Nongovernmental sources, such as John Hopkins University, stopped reporting pandemic data in March, The New York Times also ended its COVID data-gathering project in March, stating that “the comprehensive real-time reporting that The Times has prioritized is no longer possible.” It will rely on reporting weekly CDC data moving forward.
Along with the tracking sites, masking and social distancing mandates have mostly disappeared. President Joe Biden signed a bipartisan bill on April 10 that ended the national emergency for COVID. While some programs will stay in place for now, such as free vaccines, treatments, and tests, that too will go away when the federal public health emergency expires on May 11. The HHS already has issued its transition roadmap.
Many Americans, meanwhile, are still on the fence about the pandemic. A Gallup poll from March shows that about half of the American public say it’s over, and about half disagree.
Are we closing up shop on COVID-19 too soon, or is it time? Not surprisingly, experts don’t agree. Some say the pandemic is now endemic – which broadly means the virus and its patterns are predictable and steady in designated regions – and that it’s critical to catch up on health needs neglected during the pandemic, such as screenings and other vaccinations
But others don’t think it’s reached that stage yet, saying that we are letting our guard down too soon and we can’t be blind to the possibility of another strong variant – or pandemic – emerging. Surveillance must continue, not decline, and be improved.
Time to move on?
In its transition roadmap released in February, the HHS notes that daily COVID reported cases are down over 90%, compared with the peak of the Omicron surge at the end of January 2022; deaths have declined by over 80%; and new hospitalizations caused by COVID have dropped by nearly 80%.
It is time to move on, said Ali Mokdad, PhD, a professor and chief strategy officer of population health at the Institute for Health Metrics and Evaluation at the University of Washington, Seattle.
“Many people were delaying a lot of medical care, because they were afraid” during COVID’s height, he said, explaining that elective surgeries were postponed, prenatal care went down, as did screenings for blood pressure and diabetes.
His institute was tracking COVID projections every week but stopped in December.
As for emerging variants, “we haven’t seen a variant that scares us since Omicron” in November 2021, said Dr. Mokdad, who agrees that COVID is endemic now. The subvariants that followed it are very similar, and the current vaccines are working.
“We can move on, but we cannot drop the ball on keeping an eye on the genetic sequencing of the virus,” he said. That will enable quick identification of new variants.
If a worrisome new variant does surface, Dr. Mokdad said, certain locations and resources will be able to gear up quickly, while others won’t be as fast, but overall the United States is in a much better position now.
Amesh Adalja, MD, a senior scholar at the Johns Hopkins Center for Health Security, Baltimore, also believes the pandemic phase is behind us
“This can’t be an emergency in perpetuity,” he said “Just because something is not a pandemic [anymore] does not mean that all activities related to it cease.”
COVID is highly unlikely to overwhelm hospitals again, and that was the main reason for the emergency declaration, he said.
“It’s not all or none – collapsing COVID-related [monitoring] activities into the routine monitoring that is done for other infectious disease should be seen as an achievement in taming the virus,” he said.
Not endemic yet
Closing up shop too early could mean we are blindsided, said Rajendram Rajnarayanan, PhD, an assistant dean of research and associate professor at the New York Institute of Technology College of Osteopathic Medicine at Arkansas State University in Jonesboro.
Already, he said, large labs have closed or scaled down as testing demand has declined, and many centers that offered community testing have also closed. Plus, home test results are often not reported.
Continued monitoring is key, he said. “You have to maintain a base level of sequencing for new variants,” he said. “Right now, the variant that is ‘top dog’ in the world is XBB.1.16.”
That’s an Omicron subvariant that the World Health Organization is currently keeping its eye on, according to a media briefing on March 29. There are about 800 sequences of it from 22 countries, mostly India, and it’s been in circulation a few months.
Dr. Rajnarayanan said he’s not overly worried about this variant, but surveillance must continue. His own breakdown of XBB.1.16 found the subvariant in 27 countries, including the United States, as of April 10.
Ideally, Dr. Rajnarayanan would suggest four areas to keep focusing on, moving forward:
- Active, random surveillance for new variants, especially in hot spots.
- Hospital surveillance and surveillance of long-term care, especially in congregate settings where people can more easily spread the virus.
- Travelers’ surveillance, now at , according to the CDC.
- Surveillance of animals such as mink and deer, because these animals can not only pick up the virus, but the virus can mutate in the animals, which could then transmit it back to people.
With less testing, baseline surveillance for new variants has declined. The other three surveillance areas need improvement, too, he said, as the reporting is often delayed.
Continued surveillance is crucial, agreed Katelyn Jetelina, PhD, an epidemiologist and data scientist who publishes a newsletter, Your Local Epidemiologist, updating developments in COVID and other pressing health issues.
“It’s a bit ironic to have a date for the end of a public health emergency; viruses don’t care about calendars,” said Dr. Jetelina, who is also director of population health analytics for the Meadows Mental Health Policy Institute. “COVID-19 is still going to be here, it’s still going to mutate,” and still cause grief for those affected. “I’m most concerned about our ability to track the virus. It’s not clear what surveillance we will still have in the states and around the globe.”
It’s a bit ironic to have a date for the end of a public health emergency; viruses don’t care about calendars.
For surveillance, she calls wastewater monitoring “the lowest-hanging fruit.” That’s because it “is not based on bias testing and has the potential to help with other outbreaks, too.” Hospitalization data is also essential, she said, as that information is the basis for public health decisions on updated vaccines and other protective measures.
While Dr. Jetelina is hopeful that COVID will someday be universally viewed as endemic, with predictable seasonal patterns, “I don’t think we are there yet. We still need to approach this virus with humility; that’s at least what I will continue to do.”
Dr. Rajnarayanan agreed that the pandemic has not yet reached endemic phase, though the situation is much improved. “Our vaccines are still protecting us from severe disease and hospitalization, and [the antiviral drug] Paxlovid is a great tool that works.”
Keeping tabs
While some data tracking has been eliminated, not all has, or will be. The CDC, as mentioned, continues to post cases, deaths, and a daily average of new hospital admissions weekly. The WHO’s dashboard tracks deaths, cases, and vaccine doses globally.
In March, the WHO updated its working definitions and tracking system for SARS-CoV-2 variants of concern and variants of interest, with goals of evaluating the sublineages independently and to classify new variants more clearly when that’s needed.
Still, WHO is considering ending its declaration of COVID as a public health emergency of international concern sometime in 2023.
Some public companies are staying vigilant. The drugstore chain Walgreens said it plans to maintain its COVID-19 Index, which launched in January 2022.
“Data regarding spread of variants is important to our understanding of viral transmission and, as new variants emerge, it will be critical to continue to track this information quickly to predict which communities are most at risk,” Anita Patel, PharmD, vice president of pharmacy services development for Walgreens, said in a statement.
The data also reinforces the importance of vaccinations and testing in helping to stop the spread of COVID-19, she said.
A version of this article first appeared on WebMD.com.
COVID caused 4.6-year drop in NYC life expectancy
Non-White demographic groups had the highest drops. Life expectancy fell to 73 years for Black New Yorkers (a 5.5-year drop from 2019) and 77.3 years for Hispanic/Latino New Yorkers (a 6-year drop.) For White New Yorkers life expectancy only fell to 80.1 years (about a 3-year drop.)
Overall, the city had a mortality rate of 241.3 deaths per 100,000 population in 2020. That’s even higher than the 228.9 deaths per 100,000 reported during the 2018 influenza pandemic, NYC Health said in a news release.
“The sharp decline in life expectancy from 2019 was largely due to the COVID-19 pandemic,” said NYC Health Commissioner Ashwin Vasan, MD.
Another factor was a 42.2% rise in unintentional drug overdoses from 2019 to 2020. Again, racial disparities were highlighted, with the drug-related death rate highest among Black New Yorkers.
The pandemic also affected the premature death rate, meaning deaths before age 65. That rate went up 48.8% from 2019 to 2020. In the 8 previous years, from 2011 to 2019, it fell 8.6%“New Yorkers’ lifespans are falling, on top of years of relative flattening before COVID, and that cannot continue,” Dr. Vasan said in a news release.
“It is the great challenge of our time, our city, and our Department to lay out an agenda for the next era of public health, to reverse these trends, and set us out on a new path where all New Yorkers can lead healthier, longer lives,” Dr. Vasan said.
A version of this article first appeared on WebMD.com.
Non-White demographic groups had the highest drops. Life expectancy fell to 73 years for Black New Yorkers (a 5.5-year drop from 2019) and 77.3 years for Hispanic/Latino New Yorkers (a 6-year drop.) For White New Yorkers life expectancy only fell to 80.1 years (about a 3-year drop.)
Overall, the city had a mortality rate of 241.3 deaths per 100,000 population in 2020. That’s even higher than the 228.9 deaths per 100,000 reported during the 2018 influenza pandemic, NYC Health said in a news release.
“The sharp decline in life expectancy from 2019 was largely due to the COVID-19 pandemic,” said NYC Health Commissioner Ashwin Vasan, MD.
Another factor was a 42.2% rise in unintentional drug overdoses from 2019 to 2020. Again, racial disparities were highlighted, with the drug-related death rate highest among Black New Yorkers.
The pandemic also affected the premature death rate, meaning deaths before age 65. That rate went up 48.8% from 2019 to 2020. In the 8 previous years, from 2011 to 2019, it fell 8.6%“New Yorkers’ lifespans are falling, on top of years of relative flattening before COVID, and that cannot continue,” Dr. Vasan said in a news release.
“It is the great challenge of our time, our city, and our Department to lay out an agenda for the next era of public health, to reverse these trends, and set us out on a new path where all New Yorkers can lead healthier, longer lives,” Dr. Vasan said.
A version of this article first appeared on WebMD.com.
Non-White demographic groups had the highest drops. Life expectancy fell to 73 years for Black New Yorkers (a 5.5-year drop from 2019) and 77.3 years for Hispanic/Latino New Yorkers (a 6-year drop.) For White New Yorkers life expectancy only fell to 80.1 years (about a 3-year drop.)
Overall, the city had a mortality rate of 241.3 deaths per 100,000 population in 2020. That’s even higher than the 228.9 deaths per 100,000 reported during the 2018 influenza pandemic, NYC Health said in a news release.
“The sharp decline in life expectancy from 2019 was largely due to the COVID-19 pandemic,” said NYC Health Commissioner Ashwin Vasan, MD.
Another factor was a 42.2% rise in unintentional drug overdoses from 2019 to 2020. Again, racial disparities were highlighted, with the drug-related death rate highest among Black New Yorkers.
The pandemic also affected the premature death rate, meaning deaths before age 65. That rate went up 48.8% from 2019 to 2020. In the 8 previous years, from 2011 to 2019, it fell 8.6%“New Yorkers’ lifespans are falling, on top of years of relative flattening before COVID, and that cannot continue,” Dr. Vasan said in a news release.
“It is the great challenge of our time, our city, and our Department to lay out an agenda for the next era of public health, to reverse these trends, and set us out on a new path where all New Yorkers can lead healthier, longer lives,” Dr. Vasan said.
A version of this article first appeared on WebMD.com.
Long COVID: ‘On par’ with heart disease, cancer, book says
Filmmaker Gez Medinger and immunologist Danny Altmann have been dubbed by British media as “COVID’s odd couple,” and they don’t mind at all. Discussing their recent book, The Long COVID Handbook, the authors lean into their animated roles: Medinger is a passionate patient-researcher and “guinea pig” (his words) in search of his own healing, and Altmann is a no-nonsense, data-driven scientist and “Professor Boring” (as he puts it).
And the message they have about the impact of long COVID is stunning.
“The clinical burden [of long COVID] is somewhere on par with the whole of heart disease all over again, or the whole of oncology all over again, which are our biggest clinical bills concurrently,” Altmann said.
The pair met early in the pandemic, after Medinger became infected during the first wave and interviewed Altmann for his YouTube channel, which has more than 5 million views.
“Danny was one of the first people from the medical establishment to sort of stand up on the parapet and wave a flag and say, ‘Hey, guys, there’s a problem here.’ And that was incredibly validating for 2 million people in the U.K. alone who were suffering with long COVID,” Medinger said.
Their relationship works, not just for publishing one of the first definitive guides to long COVID, but also as a model for how patients with lived experiences can lead the way in medicine – from giving the condition its name to driving the medical establishment for recognition, clinical research, and therapeutic answers.
With Altmann currently leading a major research project at Imperial College London on long COVID and Medinger’s social media platform and communication skills, they’re both advancing the world’s understanding of the disease in their own way.
“We’re now more than 3 years into this completely mysterious, uncharted disease process with a whole globe full of really desperate people,” said Altmann. “It’s a living, organic thing, and yet that also demands some kind of order and collation and pulling together into some kind of sense. So I was very pleased when Gez approached me to help him with the book.”
In it, they translate everything they’ve learned about the condition that’s “scattered in 100,000 places around the globe” into a digestible format. It tells two sides of the same story: the anecdotal experiences Medinger has undergone or observed in the long COVID community through more than a dozen of his own patient-led studies, as well the hard science and research that’s amassing in the medical world.
In an interview,
What are the book’s key takeaways for you?
Medinger: “I would say we put together an incredibly comprehensive couple of chapters on the hypotheses, big picture, what’s causing long COVID. And then the nitty-gritty research for everything that we’ve found out that is going on. ... And the other part of the book that I think is particularly important, beyond the tips for managing symptoms, is the content on mental health and the impact on your emotional state and your capacity and just how huge that is. ... That has been the most powerful thing for patients when they’ve read it. And they’ve said that they’ve just been crying all the way through those chapters because suddenly they feel heard and seen.”
Altmann: “Obviously, you’d expect me to say that the parts of the book that I love most are the kind of hard-nosed, medical, mechanistic bits. ... We’ve got 150 million-plus desperate people deciding or not deciding to go and see their general practitioner, getting a fair hearing or not getting a fair hearing. And the poor doctor has never learned this in medical school, has never read a textbook on it, and hasn’t a clue what’s coming through the door.
How are they expected to know what to do? So I think the least we can do in some of those chapters is feed into their knowledge of general medicine and give them some clues. ... I think if we can explain to people what might be going on in them, and to their doctors, what on earth they might do about it, what kind of tests they might order, that helps a bit.”
How did you balance the more controversial parts of the book, including the chapter about so-called “treatments”? For instance, the book recounts Gez’s harrowing experience with ivermectin as a frightening warning. But Danny, you were nervous about even mentioning unproven and potentially dangerous treatments as things people have tried and have looked into.
Medinger: “We had to try and work out how to handle the topic, how to handle those points of view, whilst at the same time still being informative. I think the book is stronger for that chapter, too. The other thing would certainly have been to just not address the subject, but it’s one of the things that people want to know the most about. And there’s also a lot of bad information floating around out there about certain treatments. Ivermectin, for example, and this is what happened to me when I tried it. ‘Don’t do it. It’s not recommended. Please don’t.’
I think it was also very important to include because that cautionary tale really applies to every single one of those treatments that people might be hearing about that hasn’t been backed up by efficacy and safety studies.”
Altmann: “I think Gez has been quite diplomatic. That chapter was, I think, a testament to the power of the book. And the biggest test of our marriage as ‘the odd couple.’ Because when I first read the first draft of what Gez had written, I said, ‘my name can’t even be on this book. Otherwise, I’ll be sacked.’
And we had to find marriage counseling after that, and a way back to write a version of that chapter that expressed both halves of those concerns in a way that did justice to those different viewpoints. And I think that makes it quite a strong chapter.”
What do you think are the most urgent next steps in the search for solving long COVID?
Medinger: “I would personally like to try and get some sort of answer on viral persistence. ... If there’s one thing that feels like it would be treatable in theory, and would make sense why we’re still getting all of these symptoms this whole time later, it’s that, so I would like to try and establish or eliminate viral persistence. So if you gave me Elon Musk’s wealth, that’s what I would throw a bunch of the money at, trying to either eliminate or establish that.
And then, you know, the other important thing is a diagnostic test. Danny always talks about how important it is. Once you have that, it helps you suddenly open the doors to all these other things that you can do. And treatment trials. Let’s throw some meds at this so that we have an educated guess at what might work and put them into high-powered, randomized, controlled trials and see if anything comes out because from the patient perspective, I don’t think any of us wants to wait for 5 years for that stuff to start happening.”
Altmann: “I completely agree. If you go to a website, like clinicaltrials.gov, you’ll find an immense number of clinical trials on COVID. There isn’t really a shortage of them, some of them better-powered to get an answer than others.”
How do you think public policy needs to adapt for long COVID, including social safety nets such as workers’ compensation and disability benefits?
Medinger: “In terms of public policy, what I would like would be some public acknowledgment that it’s real from government sources. Just the acknowledgment that it’s real and it remains a risk even now.”
Altmann: “Nobody in politics asks my opinion. I think they’d hate to hear it. Because if I went to see them and said, well, actually, if you thought the COVID pandemic was bad, wait till you see what’s on the table now. We’ve created a disabled population in our country of 2 million, at least a portion if not more of people who are not fully contributory to the workforce anymore ... [with] legal wrangles about retirement and health insurance and pensions, and a human right to adequate health care. Which means, ideally, a purpose-built clinic where they can have their respiratory opinion and their rheumatology opinion and their endocrine opinion and their neurology opinion, all under one roof.”
You’ve both shown so much optimism. Why is that?
Altmann: “I’ve been an immunologist for a long time now, and written all my decades of grant applications, where as a community we made what, at the time, were kind of wild promises and wildly optimistic projections of how our knowledge of tumor immunity would revolutionize cancer care, and how knowledge of autoimmunity would revolutionize care of all the autoimmune diseases.
And weirdly almost every word we wrote over those 25 or 30 years came true. Cancer immunotherapy was revolutionized, and biologics for diabetes, multiple sclerosis, and arthritis were revolutionized. So if I have faith that those things came true, I have complete faith in this as well.”
Medinger: “From the patient perspective, what I would say is that we are seeing people who’ve been ill for more than 2 years recover. People are suddenly turning the corner when they might not have expected to.
And while we don’t quite know exactly why yet, and it’s not everyone, every single time I hear the story of someone saying, ‘I’m pretty much back to where I was, I feel like I’ve recovered,’ I feel great. Even if I haven’t. Because I know that every single time I hear someone say that, that just increases the probability that I will, too.”
A version of this article first appeared on WebMD.com.
Filmmaker Gez Medinger and immunologist Danny Altmann have been dubbed by British media as “COVID’s odd couple,” and they don’t mind at all. Discussing their recent book, The Long COVID Handbook, the authors lean into their animated roles: Medinger is a passionate patient-researcher and “guinea pig” (his words) in search of his own healing, and Altmann is a no-nonsense, data-driven scientist and “Professor Boring” (as he puts it).
And the message they have about the impact of long COVID is stunning.
“The clinical burden [of long COVID] is somewhere on par with the whole of heart disease all over again, or the whole of oncology all over again, which are our biggest clinical bills concurrently,” Altmann said.
The pair met early in the pandemic, after Medinger became infected during the first wave and interviewed Altmann for his YouTube channel, which has more than 5 million views.
“Danny was one of the first people from the medical establishment to sort of stand up on the parapet and wave a flag and say, ‘Hey, guys, there’s a problem here.’ And that was incredibly validating for 2 million people in the U.K. alone who were suffering with long COVID,” Medinger said.
Their relationship works, not just for publishing one of the first definitive guides to long COVID, but also as a model for how patients with lived experiences can lead the way in medicine – from giving the condition its name to driving the medical establishment for recognition, clinical research, and therapeutic answers.
With Altmann currently leading a major research project at Imperial College London on long COVID and Medinger’s social media platform and communication skills, they’re both advancing the world’s understanding of the disease in their own way.
“We’re now more than 3 years into this completely mysterious, uncharted disease process with a whole globe full of really desperate people,” said Altmann. “It’s a living, organic thing, and yet that also demands some kind of order and collation and pulling together into some kind of sense. So I was very pleased when Gez approached me to help him with the book.”
In it, they translate everything they’ve learned about the condition that’s “scattered in 100,000 places around the globe” into a digestible format. It tells two sides of the same story: the anecdotal experiences Medinger has undergone or observed in the long COVID community through more than a dozen of his own patient-led studies, as well the hard science and research that’s amassing in the medical world.
In an interview,
What are the book’s key takeaways for you?
Medinger: “I would say we put together an incredibly comprehensive couple of chapters on the hypotheses, big picture, what’s causing long COVID. And then the nitty-gritty research for everything that we’ve found out that is going on. ... And the other part of the book that I think is particularly important, beyond the tips for managing symptoms, is the content on mental health and the impact on your emotional state and your capacity and just how huge that is. ... That has been the most powerful thing for patients when they’ve read it. And they’ve said that they’ve just been crying all the way through those chapters because suddenly they feel heard and seen.”
Altmann: “Obviously, you’d expect me to say that the parts of the book that I love most are the kind of hard-nosed, medical, mechanistic bits. ... We’ve got 150 million-plus desperate people deciding or not deciding to go and see their general practitioner, getting a fair hearing or not getting a fair hearing. And the poor doctor has never learned this in medical school, has never read a textbook on it, and hasn’t a clue what’s coming through the door.
How are they expected to know what to do? So I think the least we can do in some of those chapters is feed into their knowledge of general medicine and give them some clues. ... I think if we can explain to people what might be going on in them, and to their doctors, what on earth they might do about it, what kind of tests they might order, that helps a bit.”
How did you balance the more controversial parts of the book, including the chapter about so-called “treatments”? For instance, the book recounts Gez’s harrowing experience with ivermectin as a frightening warning. But Danny, you were nervous about even mentioning unproven and potentially dangerous treatments as things people have tried and have looked into.
Medinger: “We had to try and work out how to handle the topic, how to handle those points of view, whilst at the same time still being informative. I think the book is stronger for that chapter, too. The other thing would certainly have been to just not address the subject, but it’s one of the things that people want to know the most about. And there’s also a lot of bad information floating around out there about certain treatments. Ivermectin, for example, and this is what happened to me when I tried it. ‘Don’t do it. It’s not recommended. Please don’t.’
I think it was also very important to include because that cautionary tale really applies to every single one of those treatments that people might be hearing about that hasn’t been backed up by efficacy and safety studies.”
Altmann: “I think Gez has been quite diplomatic. That chapter was, I think, a testament to the power of the book. And the biggest test of our marriage as ‘the odd couple.’ Because when I first read the first draft of what Gez had written, I said, ‘my name can’t even be on this book. Otherwise, I’ll be sacked.’
And we had to find marriage counseling after that, and a way back to write a version of that chapter that expressed both halves of those concerns in a way that did justice to those different viewpoints. And I think that makes it quite a strong chapter.”
What do you think are the most urgent next steps in the search for solving long COVID?
Medinger: “I would personally like to try and get some sort of answer on viral persistence. ... If there’s one thing that feels like it would be treatable in theory, and would make sense why we’re still getting all of these symptoms this whole time later, it’s that, so I would like to try and establish or eliminate viral persistence. So if you gave me Elon Musk’s wealth, that’s what I would throw a bunch of the money at, trying to either eliminate or establish that.
And then, you know, the other important thing is a diagnostic test. Danny always talks about how important it is. Once you have that, it helps you suddenly open the doors to all these other things that you can do. And treatment trials. Let’s throw some meds at this so that we have an educated guess at what might work and put them into high-powered, randomized, controlled trials and see if anything comes out because from the patient perspective, I don’t think any of us wants to wait for 5 years for that stuff to start happening.”
Altmann: “I completely agree. If you go to a website, like clinicaltrials.gov, you’ll find an immense number of clinical trials on COVID. There isn’t really a shortage of them, some of them better-powered to get an answer than others.”
How do you think public policy needs to adapt for long COVID, including social safety nets such as workers’ compensation and disability benefits?
Medinger: “In terms of public policy, what I would like would be some public acknowledgment that it’s real from government sources. Just the acknowledgment that it’s real and it remains a risk even now.”
Altmann: “Nobody in politics asks my opinion. I think they’d hate to hear it. Because if I went to see them and said, well, actually, if you thought the COVID pandemic was bad, wait till you see what’s on the table now. We’ve created a disabled population in our country of 2 million, at least a portion if not more of people who are not fully contributory to the workforce anymore ... [with] legal wrangles about retirement and health insurance and pensions, and a human right to adequate health care. Which means, ideally, a purpose-built clinic where they can have their respiratory opinion and their rheumatology opinion and their endocrine opinion and their neurology opinion, all under one roof.”
You’ve both shown so much optimism. Why is that?
Altmann: “I’ve been an immunologist for a long time now, and written all my decades of grant applications, where as a community we made what, at the time, were kind of wild promises and wildly optimistic projections of how our knowledge of tumor immunity would revolutionize cancer care, and how knowledge of autoimmunity would revolutionize care of all the autoimmune diseases.
And weirdly almost every word we wrote over those 25 or 30 years came true. Cancer immunotherapy was revolutionized, and biologics for diabetes, multiple sclerosis, and arthritis were revolutionized. So if I have faith that those things came true, I have complete faith in this as well.”
Medinger: “From the patient perspective, what I would say is that we are seeing people who’ve been ill for more than 2 years recover. People are suddenly turning the corner when they might not have expected to.
And while we don’t quite know exactly why yet, and it’s not everyone, every single time I hear the story of someone saying, ‘I’m pretty much back to where I was, I feel like I’ve recovered,’ I feel great. Even if I haven’t. Because I know that every single time I hear someone say that, that just increases the probability that I will, too.”
A version of this article first appeared on WebMD.com.
Filmmaker Gez Medinger and immunologist Danny Altmann have been dubbed by British media as “COVID’s odd couple,” and they don’t mind at all. Discussing their recent book, The Long COVID Handbook, the authors lean into their animated roles: Medinger is a passionate patient-researcher and “guinea pig” (his words) in search of his own healing, and Altmann is a no-nonsense, data-driven scientist and “Professor Boring” (as he puts it).
And the message they have about the impact of long COVID is stunning.
“The clinical burden [of long COVID] is somewhere on par with the whole of heart disease all over again, or the whole of oncology all over again, which are our biggest clinical bills concurrently,” Altmann said.
The pair met early in the pandemic, after Medinger became infected during the first wave and interviewed Altmann for his YouTube channel, which has more than 5 million views.
“Danny was one of the first people from the medical establishment to sort of stand up on the parapet and wave a flag and say, ‘Hey, guys, there’s a problem here.’ And that was incredibly validating for 2 million people in the U.K. alone who were suffering with long COVID,” Medinger said.
Their relationship works, not just for publishing one of the first definitive guides to long COVID, but also as a model for how patients with lived experiences can lead the way in medicine – from giving the condition its name to driving the medical establishment for recognition, clinical research, and therapeutic answers.
With Altmann currently leading a major research project at Imperial College London on long COVID and Medinger’s social media platform and communication skills, they’re both advancing the world’s understanding of the disease in their own way.
“We’re now more than 3 years into this completely mysterious, uncharted disease process with a whole globe full of really desperate people,” said Altmann. “It’s a living, organic thing, and yet that also demands some kind of order and collation and pulling together into some kind of sense. So I was very pleased when Gez approached me to help him with the book.”
In it, they translate everything they’ve learned about the condition that’s “scattered in 100,000 places around the globe” into a digestible format. It tells two sides of the same story: the anecdotal experiences Medinger has undergone or observed in the long COVID community through more than a dozen of his own patient-led studies, as well the hard science and research that’s amassing in the medical world.
In an interview,
What are the book’s key takeaways for you?
Medinger: “I would say we put together an incredibly comprehensive couple of chapters on the hypotheses, big picture, what’s causing long COVID. And then the nitty-gritty research for everything that we’ve found out that is going on. ... And the other part of the book that I think is particularly important, beyond the tips for managing symptoms, is the content on mental health and the impact on your emotional state and your capacity and just how huge that is. ... That has been the most powerful thing for patients when they’ve read it. And they’ve said that they’ve just been crying all the way through those chapters because suddenly they feel heard and seen.”
Altmann: “Obviously, you’d expect me to say that the parts of the book that I love most are the kind of hard-nosed, medical, mechanistic bits. ... We’ve got 150 million-plus desperate people deciding or not deciding to go and see their general practitioner, getting a fair hearing or not getting a fair hearing. And the poor doctor has never learned this in medical school, has never read a textbook on it, and hasn’t a clue what’s coming through the door.
How are they expected to know what to do? So I think the least we can do in some of those chapters is feed into their knowledge of general medicine and give them some clues. ... I think if we can explain to people what might be going on in them, and to their doctors, what on earth they might do about it, what kind of tests they might order, that helps a bit.”
How did you balance the more controversial parts of the book, including the chapter about so-called “treatments”? For instance, the book recounts Gez’s harrowing experience with ivermectin as a frightening warning. But Danny, you were nervous about even mentioning unproven and potentially dangerous treatments as things people have tried and have looked into.
Medinger: “We had to try and work out how to handle the topic, how to handle those points of view, whilst at the same time still being informative. I think the book is stronger for that chapter, too. The other thing would certainly have been to just not address the subject, but it’s one of the things that people want to know the most about. And there’s also a lot of bad information floating around out there about certain treatments. Ivermectin, for example, and this is what happened to me when I tried it. ‘Don’t do it. It’s not recommended. Please don’t.’
I think it was also very important to include because that cautionary tale really applies to every single one of those treatments that people might be hearing about that hasn’t been backed up by efficacy and safety studies.”
Altmann: “I think Gez has been quite diplomatic. That chapter was, I think, a testament to the power of the book. And the biggest test of our marriage as ‘the odd couple.’ Because when I first read the first draft of what Gez had written, I said, ‘my name can’t even be on this book. Otherwise, I’ll be sacked.’
And we had to find marriage counseling after that, and a way back to write a version of that chapter that expressed both halves of those concerns in a way that did justice to those different viewpoints. And I think that makes it quite a strong chapter.”
What do you think are the most urgent next steps in the search for solving long COVID?
Medinger: “I would personally like to try and get some sort of answer on viral persistence. ... If there’s one thing that feels like it would be treatable in theory, and would make sense why we’re still getting all of these symptoms this whole time later, it’s that, so I would like to try and establish or eliminate viral persistence. So if you gave me Elon Musk’s wealth, that’s what I would throw a bunch of the money at, trying to either eliminate or establish that.
And then, you know, the other important thing is a diagnostic test. Danny always talks about how important it is. Once you have that, it helps you suddenly open the doors to all these other things that you can do. And treatment trials. Let’s throw some meds at this so that we have an educated guess at what might work and put them into high-powered, randomized, controlled trials and see if anything comes out because from the patient perspective, I don’t think any of us wants to wait for 5 years for that stuff to start happening.”
Altmann: “I completely agree. If you go to a website, like clinicaltrials.gov, you’ll find an immense number of clinical trials on COVID. There isn’t really a shortage of them, some of them better-powered to get an answer than others.”
How do you think public policy needs to adapt for long COVID, including social safety nets such as workers’ compensation and disability benefits?
Medinger: “In terms of public policy, what I would like would be some public acknowledgment that it’s real from government sources. Just the acknowledgment that it’s real and it remains a risk even now.”
Altmann: “Nobody in politics asks my opinion. I think they’d hate to hear it. Because if I went to see them and said, well, actually, if you thought the COVID pandemic was bad, wait till you see what’s on the table now. We’ve created a disabled population in our country of 2 million, at least a portion if not more of people who are not fully contributory to the workforce anymore ... [with] legal wrangles about retirement and health insurance and pensions, and a human right to adequate health care. Which means, ideally, a purpose-built clinic where they can have their respiratory opinion and their rheumatology opinion and their endocrine opinion and their neurology opinion, all under one roof.”
You’ve both shown so much optimism. Why is that?
Altmann: “I’ve been an immunologist for a long time now, and written all my decades of grant applications, where as a community we made what, at the time, were kind of wild promises and wildly optimistic projections of how our knowledge of tumor immunity would revolutionize cancer care, and how knowledge of autoimmunity would revolutionize care of all the autoimmune diseases.
And weirdly almost every word we wrote over those 25 or 30 years came true. Cancer immunotherapy was revolutionized, and biologics for diabetes, multiple sclerosis, and arthritis were revolutionized. So if I have faith that those things came true, I have complete faith in this as well.”
Medinger: “From the patient perspective, what I would say is that we are seeing people who’ve been ill for more than 2 years recover. People are suddenly turning the corner when they might not have expected to.
And while we don’t quite know exactly why yet, and it’s not everyone, every single time I hear the story of someone saying, ‘I’m pretty much back to where I was, I feel like I’ve recovered,’ I feel great. Even if I haven’t. Because I know that every single time I hear someone say that, that just increases the probability that I will, too.”
A version of this article first appeared on WebMD.com.
Parents of patients with rheumatic disease, MIS-C strongly hesitant of COVID vaccination
NEW ORLEANS – Parents’ concerns about vaccinating their children against COVID-19 remain a substantial barrier to immunizing children against the disease, whether those children have chronic rheumatologic conditions or a history of multisystem inflammatory syndrome in children (MIS-C), according to two studies presented at the Pediatric Rheumatology Symposium.
Parents of children who developed MIS-C after a SARS-CoV-2 infection were particularly hesitant to vaccinate, despite strong encouragement from health care professionals at Baylor College of Medicine, Houston, said the presenter of one of the studies.
“Unfortunately, it remains unclear who is susceptible and what the mechanisms are” when it comes to MIS-C, Mariana Sanchez Villa, MS, a research coordinator at Baylor, told attendees. “Because of this, there is much hesitancy to vaccinate children with a history of MIS-C against COVID-19 out of a fear that hyperinflammation may occur.”
Ms. Sanchez Villa reported findings on the vaccination rate among patients who had been hospitalized with MIS-C. The researchers included all 295 patients who presented at the hospital with MIS-C between May 2020 and October 2022. Overall, 5% of these patients had been vaccinated against COVID-19 before they were diagnosed with MIS-C. When all these patients and their families came to outpatient follow-up appointments after discharge, the subspecialist clinicians recommended the children receive the COVID-19 vaccine 3 months after discharge. The researchers then reviewed the patients’ charts to see who did and did not receive the vaccine, which they confirmed through the state’s immunization registry.
Among the 295 patients with MIS-C, 1 died, and 99 (34%) received at least one COVID-19 vaccine dose after their diagnosis, including 7 of the 15 who had also been vaccinated prior to their MIS-C diagnosis. Just over half of the vaccinated patients (58%) were male. They received their vaccine an average 8.8 months after their hospitalization, when they were an average 10 years old, and all but one of the vaccine doses they received were the Pfizer/BioNTech mRNA vaccine.
Only 9 of the 99 vaccinated patients are fully vaccinated, defined as receiving the primary series plus the recommended boosters. Of the other patients, 13 received only one dose of the vaccine, 60 received two doses, and 17 received at least three doses of the primary series doses but no bivalent boosters. Over a subsequent average 11 months of follow-up, none of the vaccinated patients returned to the hospital with a recurrence of MIS-C or any other hyperinflammatory condition. The seven patients who had been vaccinated both before and after their MIS-C diagnosis have also not had any recurrence of a hyperinflammatory condition.
“SARS-CoV-2 vaccination is well-tolerated by children with a history of MIS-C,” the researchers concluded. Ms. Sanchez Villa referenced two other studies, in The Pediatric Infectious Disease Journal and in JAMA Network Open, with similar findings on the safety of COVID-19 vaccination in patients who have had MIS-C. “This is reassuring as SARS-CoV-2 becomes endemic and annual vaccination against SARS-CoV-2 is considered.”
Dilan Dissanayake, MD, PhD, a rheumatologist at The Hospital for Sick Children in Toronto, who attended the presentation, told this news organization that data increasingly show a “synergistic protective effect” from COVID-19 infection and vaccination. That is, “having COVID or having MIS-C once doesn’t necessarily preclude you from having it again,” thereby supporting the importance of vaccination after an MIS-C diagnosis. In talking to parents about vaccinating, he has found it most helpful for them to hear about rheumatologists’ experience regarding COVID-19 vaccination.
“Particularly as the pandemic went on, being able to comfortably say that we have this large patient group, as well as collaborators across the world who have been monitoring for any safety issues, and that all the data has been reassuring” has been most useful for parents to hear, Dr. Dissanayake said.
The other study, led by Beth Rutstein, MD, MSCE, an attending rheumatologist at Children’s Hospital of Philadelphia, focused on the population of pediatric rheumatology patients by surveying pediatric rheumatologists who were members of the Childhood Arthritis and Rheumatology Research Alliance. The survey, conducted from March to May 2022, included questions about the rheumatologists’ COVID-19 vaccination practices as well as perceptions of the vaccine by the parents of their patients.
The 219 respondents included 74% pediatric rheumatologists and 21% fellows. Nearly all the respondents (98%) believed that any disease flares after COVID-19 vaccination would be mild and/or rare, and nearly all (98%) recommend their patients be vaccinated against COVID-19.
The primary finding from the study was that “we [rheumatologists] have different concerns from the families,” coauthor and presenter Vidya Sivaraman, MD, a pediatric rheumatologist at Nationwide Children’s Hospital and the Ohio State University in Columbus, told this news organization. “We’re more worried about the efficacy of the vaccine on immunosuppressive medications,” such as rituximab, which depletes B cells, Dr. Sivaraman said, but concerns about the vaccine’s immunogenicity or efficacy were very low among parents.
Just over half the clinicians surveyed (59%) were concerned about how effective the vaccine would be for their patients, especially those receiving immunosuppressive therapy. Health care professionals were most concerned about patients on rituximab – all clinicians reported concerns about the vaccine’s effectiveness in these patients – followed by patients taking systemic corticosteroids (86%), mycophenolate mofetil (59%), and Janus kinase inhibitors (46%).
Most clinicians (88%) reported that they had temporarily modified a patient’s immunosuppressive therapy to allow for vaccination, following guidelines by the American College of Rheumatology. Aside from a small proportion of health care professionals who checked patients’ post-vaccination serology primarily for research purposes, most clinicians (82%) did not collect this serology.
In regard to adverse events, the concern cited most often by respondents was myocarditis (76%), followed by development of new autoimmune conditions (29%) and thrombosis (22%), but the clinicians ranked these adverse events as low risk.
Meanwhile, the top three concerns about vaccination among parents, as reported to physicians, were worries about side effects, lack of long-term safety data on the vaccine, and misinformation they had heard, such as anxiety about changes to their child’s genetics or vaccination causing a COVID-19 infection. “They’re seeing things on social media from other parents [saying that COVID-19 vaccines are] going to affect their fertility, so they don’t want their daughters to get it,” Dr. Sivaraman said as another example of commonly cited misinformation.
Nearly half of the respondents (47%) said more than half of their families had concerns about side effects and the lack of data on long-term outcomes after vaccination. Only 8.5% of physicians said that fewer than 10% of their families were anxious about side effects. In addition, 39% of physicians said more than half of their families had concerns about misinformation they had heard, and only 16% of physicians had heard about misinformation concerns from fewer than 10% of their patients.
Other concerns cited by parents included their child’s disease flaring; lack of data on how well the vaccine would stimulate their child’s immune system; their child having already had COVID-19; and not believing COVID-19 was a major health risk to their child. Nearly every respondent (98%) said they had parents who turned down COVID-19 vaccination, and a majority (75%) reported that more than 10% of their patients had parents who were hesitant about COVID-19 vaccination.
No external funding was noted for either study. Ms. Sanchez Villa had no relevant financial relationships, but two abstract coauthors reported financial relationships with Pfizer and Moderna, and one reported a financial relationship with Novartis. Dr. Rutstein, Dr. Sivaraman, and Dr. Dissanayake had no relevant financial relationships.
A version of this article first appeared on Medscape.com.
NEW ORLEANS – Parents’ concerns about vaccinating their children against COVID-19 remain a substantial barrier to immunizing children against the disease, whether those children have chronic rheumatologic conditions or a history of multisystem inflammatory syndrome in children (MIS-C), according to two studies presented at the Pediatric Rheumatology Symposium.
Parents of children who developed MIS-C after a SARS-CoV-2 infection were particularly hesitant to vaccinate, despite strong encouragement from health care professionals at Baylor College of Medicine, Houston, said the presenter of one of the studies.
“Unfortunately, it remains unclear who is susceptible and what the mechanisms are” when it comes to MIS-C, Mariana Sanchez Villa, MS, a research coordinator at Baylor, told attendees. “Because of this, there is much hesitancy to vaccinate children with a history of MIS-C against COVID-19 out of a fear that hyperinflammation may occur.”
Ms. Sanchez Villa reported findings on the vaccination rate among patients who had been hospitalized with MIS-C. The researchers included all 295 patients who presented at the hospital with MIS-C between May 2020 and October 2022. Overall, 5% of these patients had been vaccinated against COVID-19 before they were diagnosed with MIS-C. When all these patients and their families came to outpatient follow-up appointments after discharge, the subspecialist clinicians recommended the children receive the COVID-19 vaccine 3 months after discharge. The researchers then reviewed the patients’ charts to see who did and did not receive the vaccine, which they confirmed through the state’s immunization registry.
Among the 295 patients with MIS-C, 1 died, and 99 (34%) received at least one COVID-19 vaccine dose after their diagnosis, including 7 of the 15 who had also been vaccinated prior to their MIS-C diagnosis. Just over half of the vaccinated patients (58%) were male. They received their vaccine an average 8.8 months after their hospitalization, when they were an average 10 years old, and all but one of the vaccine doses they received were the Pfizer/BioNTech mRNA vaccine.
Only 9 of the 99 vaccinated patients are fully vaccinated, defined as receiving the primary series plus the recommended boosters. Of the other patients, 13 received only one dose of the vaccine, 60 received two doses, and 17 received at least three doses of the primary series doses but no bivalent boosters. Over a subsequent average 11 months of follow-up, none of the vaccinated patients returned to the hospital with a recurrence of MIS-C or any other hyperinflammatory condition. The seven patients who had been vaccinated both before and after their MIS-C diagnosis have also not had any recurrence of a hyperinflammatory condition.
“SARS-CoV-2 vaccination is well-tolerated by children with a history of MIS-C,” the researchers concluded. Ms. Sanchez Villa referenced two other studies, in The Pediatric Infectious Disease Journal and in JAMA Network Open, with similar findings on the safety of COVID-19 vaccination in patients who have had MIS-C. “This is reassuring as SARS-CoV-2 becomes endemic and annual vaccination against SARS-CoV-2 is considered.”
Dilan Dissanayake, MD, PhD, a rheumatologist at The Hospital for Sick Children in Toronto, who attended the presentation, told this news organization that data increasingly show a “synergistic protective effect” from COVID-19 infection and vaccination. That is, “having COVID or having MIS-C once doesn’t necessarily preclude you from having it again,” thereby supporting the importance of vaccination after an MIS-C diagnosis. In talking to parents about vaccinating, he has found it most helpful for them to hear about rheumatologists’ experience regarding COVID-19 vaccination.
“Particularly as the pandemic went on, being able to comfortably say that we have this large patient group, as well as collaborators across the world who have been monitoring for any safety issues, and that all the data has been reassuring” has been most useful for parents to hear, Dr. Dissanayake said.
The other study, led by Beth Rutstein, MD, MSCE, an attending rheumatologist at Children’s Hospital of Philadelphia, focused on the population of pediatric rheumatology patients by surveying pediatric rheumatologists who were members of the Childhood Arthritis and Rheumatology Research Alliance. The survey, conducted from March to May 2022, included questions about the rheumatologists’ COVID-19 vaccination practices as well as perceptions of the vaccine by the parents of their patients.
The 219 respondents included 74% pediatric rheumatologists and 21% fellows. Nearly all the respondents (98%) believed that any disease flares after COVID-19 vaccination would be mild and/or rare, and nearly all (98%) recommend their patients be vaccinated against COVID-19.
The primary finding from the study was that “we [rheumatologists] have different concerns from the families,” coauthor and presenter Vidya Sivaraman, MD, a pediatric rheumatologist at Nationwide Children’s Hospital and the Ohio State University in Columbus, told this news organization. “We’re more worried about the efficacy of the vaccine on immunosuppressive medications,” such as rituximab, which depletes B cells, Dr. Sivaraman said, but concerns about the vaccine’s immunogenicity or efficacy were very low among parents.
Just over half the clinicians surveyed (59%) were concerned about how effective the vaccine would be for their patients, especially those receiving immunosuppressive therapy. Health care professionals were most concerned about patients on rituximab – all clinicians reported concerns about the vaccine’s effectiveness in these patients – followed by patients taking systemic corticosteroids (86%), mycophenolate mofetil (59%), and Janus kinase inhibitors (46%).
Most clinicians (88%) reported that they had temporarily modified a patient’s immunosuppressive therapy to allow for vaccination, following guidelines by the American College of Rheumatology. Aside from a small proportion of health care professionals who checked patients’ post-vaccination serology primarily for research purposes, most clinicians (82%) did not collect this serology.
In regard to adverse events, the concern cited most often by respondents was myocarditis (76%), followed by development of new autoimmune conditions (29%) and thrombosis (22%), but the clinicians ranked these adverse events as low risk.
Meanwhile, the top three concerns about vaccination among parents, as reported to physicians, were worries about side effects, lack of long-term safety data on the vaccine, and misinformation they had heard, such as anxiety about changes to their child’s genetics or vaccination causing a COVID-19 infection. “They’re seeing things on social media from other parents [saying that COVID-19 vaccines are] going to affect their fertility, so they don’t want their daughters to get it,” Dr. Sivaraman said as another example of commonly cited misinformation.
Nearly half of the respondents (47%) said more than half of their families had concerns about side effects and the lack of data on long-term outcomes after vaccination. Only 8.5% of physicians said that fewer than 10% of their families were anxious about side effects. In addition, 39% of physicians said more than half of their families had concerns about misinformation they had heard, and only 16% of physicians had heard about misinformation concerns from fewer than 10% of their patients.
Other concerns cited by parents included their child’s disease flaring; lack of data on how well the vaccine would stimulate their child’s immune system; their child having already had COVID-19; and not believing COVID-19 was a major health risk to their child. Nearly every respondent (98%) said they had parents who turned down COVID-19 vaccination, and a majority (75%) reported that more than 10% of their patients had parents who were hesitant about COVID-19 vaccination.
No external funding was noted for either study. Ms. Sanchez Villa had no relevant financial relationships, but two abstract coauthors reported financial relationships with Pfizer and Moderna, and one reported a financial relationship with Novartis. Dr. Rutstein, Dr. Sivaraman, and Dr. Dissanayake had no relevant financial relationships.
A version of this article first appeared on Medscape.com.
NEW ORLEANS – Parents’ concerns about vaccinating their children against COVID-19 remain a substantial barrier to immunizing children against the disease, whether those children have chronic rheumatologic conditions or a history of multisystem inflammatory syndrome in children (MIS-C), according to two studies presented at the Pediatric Rheumatology Symposium.
Parents of children who developed MIS-C after a SARS-CoV-2 infection were particularly hesitant to vaccinate, despite strong encouragement from health care professionals at Baylor College of Medicine, Houston, said the presenter of one of the studies.
“Unfortunately, it remains unclear who is susceptible and what the mechanisms are” when it comes to MIS-C, Mariana Sanchez Villa, MS, a research coordinator at Baylor, told attendees. “Because of this, there is much hesitancy to vaccinate children with a history of MIS-C against COVID-19 out of a fear that hyperinflammation may occur.”
Ms. Sanchez Villa reported findings on the vaccination rate among patients who had been hospitalized with MIS-C. The researchers included all 295 patients who presented at the hospital with MIS-C between May 2020 and October 2022. Overall, 5% of these patients had been vaccinated against COVID-19 before they were diagnosed with MIS-C. When all these patients and their families came to outpatient follow-up appointments after discharge, the subspecialist clinicians recommended the children receive the COVID-19 vaccine 3 months after discharge. The researchers then reviewed the patients’ charts to see who did and did not receive the vaccine, which they confirmed through the state’s immunization registry.
Among the 295 patients with MIS-C, 1 died, and 99 (34%) received at least one COVID-19 vaccine dose after their diagnosis, including 7 of the 15 who had also been vaccinated prior to their MIS-C diagnosis. Just over half of the vaccinated patients (58%) were male. They received their vaccine an average 8.8 months after their hospitalization, when they were an average 10 years old, and all but one of the vaccine doses they received were the Pfizer/BioNTech mRNA vaccine.
Only 9 of the 99 vaccinated patients are fully vaccinated, defined as receiving the primary series plus the recommended boosters. Of the other patients, 13 received only one dose of the vaccine, 60 received two doses, and 17 received at least three doses of the primary series doses but no bivalent boosters. Over a subsequent average 11 months of follow-up, none of the vaccinated patients returned to the hospital with a recurrence of MIS-C or any other hyperinflammatory condition. The seven patients who had been vaccinated both before and after their MIS-C diagnosis have also not had any recurrence of a hyperinflammatory condition.
“SARS-CoV-2 vaccination is well-tolerated by children with a history of MIS-C,” the researchers concluded. Ms. Sanchez Villa referenced two other studies, in The Pediatric Infectious Disease Journal and in JAMA Network Open, with similar findings on the safety of COVID-19 vaccination in patients who have had MIS-C. “This is reassuring as SARS-CoV-2 becomes endemic and annual vaccination against SARS-CoV-2 is considered.”
Dilan Dissanayake, MD, PhD, a rheumatologist at The Hospital for Sick Children in Toronto, who attended the presentation, told this news organization that data increasingly show a “synergistic protective effect” from COVID-19 infection and vaccination. That is, “having COVID or having MIS-C once doesn’t necessarily preclude you from having it again,” thereby supporting the importance of vaccination after an MIS-C diagnosis. In talking to parents about vaccinating, he has found it most helpful for them to hear about rheumatologists’ experience regarding COVID-19 vaccination.
“Particularly as the pandemic went on, being able to comfortably say that we have this large patient group, as well as collaborators across the world who have been monitoring for any safety issues, and that all the data has been reassuring” has been most useful for parents to hear, Dr. Dissanayake said.
The other study, led by Beth Rutstein, MD, MSCE, an attending rheumatologist at Children’s Hospital of Philadelphia, focused on the population of pediatric rheumatology patients by surveying pediatric rheumatologists who were members of the Childhood Arthritis and Rheumatology Research Alliance. The survey, conducted from March to May 2022, included questions about the rheumatologists’ COVID-19 vaccination practices as well as perceptions of the vaccine by the parents of their patients.
The 219 respondents included 74% pediatric rheumatologists and 21% fellows. Nearly all the respondents (98%) believed that any disease flares after COVID-19 vaccination would be mild and/or rare, and nearly all (98%) recommend their patients be vaccinated against COVID-19.
The primary finding from the study was that “we [rheumatologists] have different concerns from the families,” coauthor and presenter Vidya Sivaraman, MD, a pediatric rheumatologist at Nationwide Children’s Hospital and the Ohio State University in Columbus, told this news organization. “We’re more worried about the efficacy of the vaccine on immunosuppressive medications,” such as rituximab, which depletes B cells, Dr. Sivaraman said, but concerns about the vaccine’s immunogenicity or efficacy were very low among parents.
Just over half the clinicians surveyed (59%) were concerned about how effective the vaccine would be for their patients, especially those receiving immunosuppressive therapy. Health care professionals were most concerned about patients on rituximab – all clinicians reported concerns about the vaccine’s effectiveness in these patients – followed by patients taking systemic corticosteroids (86%), mycophenolate mofetil (59%), and Janus kinase inhibitors (46%).
Most clinicians (88%) reported that they had temporarily modified a patient’s immunosuppressive therapy to allow for vaccination, following guidelines by the American College of Rheumatology. Aside from a small proportion of health care professionals who checked patients’ post-vaccination serology primarily for research purposes, most clinicians (82%) did not collect this serology.
In regard to adverse events, the concern cited most often by respondents was myocarditis (76%), followed by development of new autoimmune conditions (29%) and thrombosis (22%), but the clinicians ranked these adverse events as low risk.
Meanwhile, the top three concerns about vaccination among parents, as reported to physicians, were worries about side effects, lack of long-term safety data on the vaccine, and misinformation they had heard, such as anxiety about changes to their child’s genetics or vaccination causing a COVID-19 infection. “They’re seeing things on social media from other parents [saying that COVID-19 vaccines are] going to affect their fertility, so they don’t want their daughters to get it,” Dr. Sivaraman said as another example of commonly cited misinformation.
Nearly half of the respondents (47%) said more than half of their families had concerns about side effects and the lack of data on long-term outcomes after vaccination. Only 8.5% of physicians said that fewer than 10% of their families were anxious about side effects. In addition, 39% of physicians said more than half of their families had concerns about misinformation they had heard, and only 16% of physicians had heard about misinformation concerns from fewer than 10% of their patients.
Other concerns cited by parents included their child’s disease flaring; lack of data on how well the vaccine would stimulate their child’s immune system; their child having already had COVID-19; and not believing COVID-19 was a major health risk to their child. Nearly every respondent (98%) said they had parents who turned down COVID-19 vaccination, and a majority (75%) reported that more than 10% of their patients had parents who were hesitant about COVID-19 vaccination.
No external funding was noted for either study. Ms. Sanchez Villa had no relevant financial relationships, but two abstract coauthors reported financial relationships with Pfizer and Moderna, and one reported a financial relationship with Novartis. Dr. Rutstein, Dr. Sivaraman, and Dr. Dissanayake had no relevant financial relationships.
A version of this article first appeared on Medscape.com.
AT PRSYM 2023