Pulmonary Health Hub

The gout drug colchicine appears to lower the severity of COVID-19, a small new Brazilian study finds, adding to evidence that the familiar medication holds promise as a treatment for hospitalized patients.

Patients who received colchicine in this randomized, double-blinded, placebo-controlled clinical trial presented better evolution in terms of the need for supplemental oxygen and the length of hospitalisation. ... Colchicine was safe and well tolerated,” the study authors wrote in RMD Open. However, deaths were rare in the trial, they added, and it is impossible to “evaluate the capacity of colchicine to avoid admission to ICU and reduce mortality.”

The oral anti-inflammatory colchicine, widely used as treatment in rheumatic disease, was first approved in the United States 60 years ago. Researchers began to explore its potential as a COVID-19 treatment in the early months of the pandemic.

On Jan. 25, an international team of researchers reported in a press release – but not yet a published paper – that the drug seemed to reduce hospitalizations, mechanical ventilation, and deaths in the ColCORONA trial. Earlier, a much-smaller, randomized, open-label, Greek trial linked the drug to reduced time to clinical deterioration and hospital stay.

The Brazilian authors of the new study, led by Maria Isabel Lopes of the University of São Paulo’s Ribeirão Preto Medical School, randomly assigned 75 hospitalized patients with moderate to severe COVID-19 to colchicine or placebo. A total of 72 subjects completed the April-August 2020 trial: 36 received colchicine (typically 0.5 mg three times for 5 days, then 0.5 mg twice daily for 5 days; doses were adjusted in low-weight patients and those with chronic kidney disease). The other 36 received the placebo.

(In the United States, 0.6-mg tablets of generic colchicine cost as little as $1.90 each with free coupons, according to goodrx.com.)

The median age in the groups was similar (55 years); and the placebo group had more women (61% vs. 47% in the colchicine group, P = .34). All 72 patients received the same COVID-19 treatment at the time of the trial: azithromycin, hydroxychloroquine, and unfractionated heparin. Most patients, about two-thirds in both groups, also received methylprednisolone because they needed higher amounts of supplemental oxygen.

Patients in the colchicine group needed supplemental oxygen for less time: Their median time of need was 4.0 days (interquartile range [IQR], 2.0-6.0) vs. 6.5 days (IQR, 4.0-9.0) for the placebo group (P < .001). The median time for hospitalization was also lower at 7.0 days (IQR, 5.0–9.0) for the colchicine group vs. 9.0 (IQR, 7.0–12.0) for the placebo group (log rank test, 10.6; P = .001).

The researchers also reported the percentage of patients who needed supplemental oxygen at day 2 as 67% with colchicine vs. 86% with placebo, and at day 7 as 9% vs. 42% (log rank test, 10.6; P = .001). Two patients in the placebo group died, both from ventilator-associated pneumonia.

As for side effects, new or worsened diarrhea was reported more often in the colchicine group (17% vs. 6% with placebo), but the difference was not statistically significant (P = .26), and diarrhea was controlled via medication.

The researchers reported that limitations include the exclusion criteria and their inability to link colchicine to rates of ICU admissions and death.

The drug appears to help patients with COVID-19, the study authors wrote, by “inhibiting inflammasome, reducing neutrophil migration and activation, or preventing endothelial damage.”

A “well-conceived and well-designed” study

In an interview, NYU Langone Health rheumatologist Michael H. Pillinger, MD – an investigator with the ColCORONA trial – praised the Brazilian study. It “appears well-conceived and well-designed, and was enrolled at a rate that was greater than the sample size that was estimated to be needed based on power analysis,” he said.

The Brazilian study is small, he noted. (In contrast, the ColCORONA trial had 4,488 outpatient participants.) “This study differs from ColCORONA in several ways – the most important being that it is a study of inpatients with moderate to severe COVID (really mostly moderate),” he added. “ColCORONA is looking at a target audience that is much larger – outpatients with mild to moderate COVID with risk factors for hospitalization. Both questions are really important and certainly not mutually exclusive, since our care remains inadequate in both venues. This study also adds value in that several other studies have been conducted in hospital patients with enrollment criteria relatively similar to this one, and all showed benefit, but those were open-label or retrospective, and this is blinded and placebo-controlled.”
 

Using colchicine in patients with COVID-19

Should physicians turn to colchicine in patients with COVID-19? “I would rather that it still be used in the context of research until formal recommendations can be made by bodies like the NIH and CDC,” Dr. Pillinger said. “But certainly, there may be times when physicians feel compelled to treat patients off label.”

He cautioned, however, that colchicine should never be used with some other drugs. Its interaction with the antibiotic clarithromycin can be fatal, he noted. And, he said, the drug must be monitored in general since it can cause rare, severe problems.

“Overall, colchicine probably works on the overabundant inflammatory response to COVID, and it may be that it can be combined with other drugs that affect viral replication or promote immunity – e.g. vaccines,” Dr. Pillinger said. “So far, it seems as if there is no safety problem with combining colchicine with other approaches, but this has not been studied in a rigorous manner.”

Moving forward, he said, the drug’s very low price outside of the United States “could provide resource-poor countries with a way to help keep patients out of precious hospital beds – or help them go home sooner once admitted.” For now, however, “we need a large-scale inpatient study, and one is currently going on in Great Britain. We also need validation of the outpatient ColCORONA study, and studies to look at whether colchicine can work in conjunction with other strategies.”

The study was funded by grants from the São Paulo Research Foundation, Brazilian National Council for Scientific and Technological Development, and CAPES Foundation. No disclosures are reported. Dr. Pillinger reports serving as an investigator for the ColCORONA trial and receiving a unrelated investigator-initiated grant from Hikma, a colchicine manufacturer.

The gout drug colchicine appears to lower the severity of COVID-19, a small new Brazilian study finds, adding to evidence that the familiar medication holds promise as a treatment for hospitalized patients.

Patients who received colchicine in this randomized, double-blinded, placebo-controlled clinical trial presented better evolution in terms of the need for supplemental oxygen and the length of hospitalisation. ... Colchicine was safe and well tolerated,” the study authors wrote in RMD Open. However, deaths were rare in the trial, they added, and it is impossible to “evaluate the capacity of colchicine to avoid admission to ICU and reduce mortality.”

The oral anti-inflammatory colchicine, widely used as treatment in rheumatic disease, was first approved in the United States 60 years ago. Researchers began to explore its potential as a COVID-19 treatment in the early months of the pandemic.

On Jan. 25, an international team of researchers reported in a press release – but not yet a published paper – that the drug seemed to reduce hospitalizations, mechanical ventilation, and deaths in the ColCORONA trial. Earlier, a much-smaller, randomized, open-label, Greek trial linked the drug to reduced time to clinical deterioration and hospital stay.

The Brazilian authors of the new study, led by Maria Isabel Lopes of the University of São Paulo’s Ribeirão Preto Medical School, randomly assigned 75 hospitalized patients with moderate to severe COVID-19 to colchicine or placebo. A total of 72 subjects completed the April-August 2020 trial: 36 received colchicine (typically 0.5 mg three times for 5 days, then 0.5 mg twice daily for 5 days; doses were adjusted in low-weight patients and those with chronic kidney disease). The other 36 received the placebo.

(In the United States, 0.6-mg tablets of generic colchicine cost as little as $1.90 each with free coupons, according to goodrx.com.)

The median age in the groups was similar (55 years); and the placebo group had more women (61% vs. 47% in the colchicine group, P = .34). All 72 patients received the same COVID-19 treatment at the time of the trial: azithromycin, hydroxychloroquine, and unfractionated heparin. Most patients, about two-thirds in both groups, also received methylprednisolone because they needed higher amounts of supplemental oxygen.

Patients in the colchicine group needed supplemental oxygen for less time: Their median time of need was 4.0 days (interquartile range [IQR], 2.0-6.0) vs. 6.5 days (IQR, 4.0-9.0) for the placebo group (P < .001). The median time for hospitalization was also lower at 7.0 days (IQR, 5.0–9.0) for the colchicine group vs. 9.0 (IQR, 7.0–12.0) for the placebo group (log rank test, 10.6; P = .001).

The researchers also reported the percentage of patients who needed supplemental oxygen at day 2 as 67% with colchicine vs. 86% with placebo, and at day 7 as 9% vs. 42% (log rank test, 10.6; P = .001). Two patients in the placebo group died, both from ventilator-associated pneumonia.

As for side effects, new or worsened diarrhea was reported more often in the colchicine group (17% vs. 6% with placebo), but the difference was not statistically significant (P = .26), and diarrhea was controlled via medication.

The researchers reported that limitations include the exclusion criteria and their inability to link colchicine to rates of ICU admissions and death.

The drug appears to help patients with COVID-19, the study authors wrote, by “inhibiting inflammasome, reducing neutrophil migration and activation, or preventing endothelial damage.”

A “well-conceived and well-designed” study

In an interview, NYU Langone Health rheumatologist Michael H. Pillinger, MD – an investigator with the ColCORONA trial – praised the Brazilian study. It “appears well-conceived and well-designed, and was enrolled at a rate that was greater than the sample size that was estimated to be needed based on power analysis,” he said.

The Brazilian study is small, he noted. (In contrast, the ColCORONA trial had 4,488 outpatient participants.) “This study differs from ColCORONA in several ways – the most important being that it is a study of inpatients with moderate to severe COVID (really mostly moderate),” he added. “ColCORONA is looking at a target audience that is much larger – outpatients with mild to moderate COVID with risk factors for hospitalization. Both questions are really important and certainly not mutually exclusive, since our care remains inadequate in both venues. This study also adds value in that several other studies have been conducted in hospital patients with enrollment criteria relatively similar to this one, and all showed benefit, but those were open-label or retrospective, and this is blinded and placebo-controlled.”
 

Using colchicine in patients with COVID-19

Should physicians turn to colchicine in patients with COVID-19? “I would rather that it still be used in the context of research until formal recommendations can be made by bodies like the NIH and CDC,” Dr. Pillinger said. “But certainly, there may be times when physicians feel compelled to treat patients off label.”

He cautioned, however, that colchicine should never be used with some other drugs. Its interaction with the antibiotic clarithromycin can be fatal, he noted. And, he said, the drug must be monitored in general since it can cause rare, severe problems.

“Overall, colchicine probably works on the overabundant inflammatory response to COVID, and it may be that it can be combined with other drugs that affect viral replication or promote immunity – e.g. vaccines,” Dr. Pillinger said. “So far, it seems as if there is no safety problem with combining colchicine with other approaches, but this has not been studied in a rigorous manner.”

Moving forward, he said, the drug’s very low price outside of the United States “could provide resource-poor countries with a way to help keep patients out of precious hospital beds – or help them go home sooner once admitted.” For now, however, “we need a large-scale inpatient study, and one is currently going on in Great Britain. We also need validation of the outpatient ColCORONA study, and studies to look at whether colchicine can work in conjunction with other strategies.”

The study was funded by grants from the São Paulo Research Foundation, Brazilian National Council for Scientific and Technological Development, and CAPES Foundation. No disclosures are reported. Dr. Pillinger reports serving as an investigator for the ColCORONA trial and receiving a unrelated investigator-initiated grant from Hikma, a colchicine manufacturer.

The gout drug colchicine appears to lower the severity of COVID-19, a small new Brazilian study finds, adding to evidence that the familiar medication holds promise as a treatment for hospitalized patients.

Patients who received colchicine in this randomized, double-blinded, placebo-controlled clinical trial presented better evolution in terms of the need for supplemental oxygen and the length of hospitalisation. ... Colchicine was safe and well tolerated,” the study authors wrote in RMD Open. However, deaths were rare in the trial, they added, and it is impossible to “evaluate the capacity of colchicine to avoid admission to ICU and reduce mortality.”

The oral anti-inflammatory colchicine, widely used as treatment in rheumatic disease, was first approved in the United States 60 years ago. Researchers began to explore its potential as a COVID-19 treatment in the early months of the pandemic.

On Jan. 25, an international team of researchers reported in a press release – but not yet a published paper – that the drug seemed to reduce hospitalizations, mechanical ventilation, and deaths in the ColCORONA trial. Earlier, a much-smaller, randomized, open-label, Greek trial linked the drug to reduced time to clinical deterioration and hospital stay.

The Brazilian authors of the new study, led by Maria Isabel Lopes of the University of São Paulo’s Ribeirão Preto Medical School, randomly assigned 75 hospitalized patients with moderate to severe COVID-19 to colchicine or placebo. A total of 72 subjects completed the April-August 2020 trial: 36 received colchicine (typically 0.5 mg three times for 5 days, then 0.5 mg twice daily for 5 days; doses were adjusted in low-weight patients and those with chronic kidney disease). The other 36 received the placebo.

(In the United States, 0.6-mg tablets of generic colchicine cost as little as $1.90 each with free coupons, according to goodrx.com.)

The median age in the groups was similar (55 years); and the placebo group had more women (61% vs. 47% in the colchicine group, P = .34). All 72 patients received the same COVID-19 treatment at the time of the trial: azithromycin, hydroxychloroquine, and unfractionated heparin. Most patients, about two-thirds in both groups, also received methylprednisolone because they needed higher amounts of supplemental oxygen.

Patients in the colchicine group needed supplemental oxygen for less time: Their median time of need was 4.0 days (interquartile range [IQR], 2.0-6.0) vs. 6.5 days (IQR, 4.0-9.0) for the placebo group (P < .001). The median time for hospitalization was also lower at 7.0 days (IQR, 5.0–9.0) for the colchicine group vs. 9.0 (IQR, 7.0–12.0) for the placebo group (log rank test, 10.6; P = .001).

The researchers also reported the percentage of patients who needed supplemental oxygen at day 2 as 67% with colchicine vs. 86% with placebo, and at day 7 as 9% vs. 42% (log rank test, 10.6; P = .001). Two patients in the placebo group died, both from ventilator-associated pneumonia.

As for side effects, new or worsened diarrhea was reported more often in the colchicine group (17% vs. 6% with placebo), but the difference was not statistically significant (P = .26), and diarrhea was controlled via medication.

The researchers reported that limitations include the exclusion criteria and their inability to link colchicine to rates of ICU admissions and death.

The drug appears to help patients with COVID-19, the study authors wrote, by “inhibiting inflammasome, reducing neutrophil migration and activation, or preventing endothelial damage.”

A “well-conceived and well-designed” study

In an interview, NYU Langone Health rheumatologist Michael H. Pillinger, MD – an investigator with the ColCORONA trial – praised the Brazilian study. It “appears well-conceived and well-designed, and was enrolled at a rate that was greater than the sample size that was estimated to be needed based on power analysis,” he said.

The Brazilian study is small, he noted. (In contrast, the ColCORONA trial had 4,488 outpatient participants.) “This study differs from ColCORONA in several ways – the most important being that it is a study of inpatients with moderate to severe COVID (really mostly moderate),” he added. “ColCORONA is looking at a target audience that is much larger – outpatients with mild to moderate COVID with risk factors for hospitalization. Both questions are really important and certainly not mutually exclusive, since our care remains inadequate in both venues. This study also adds value in that several other studies have been conducted in hospital patients with enrollment criteria relatively similar to this one, and all showed benefit, but those were open-label or retrospective, and this is blinded and placebo-controlled.”
 

Using colchicine in patients with COVID-19

Should physicians turn to colchicine in patients with COVID-19? “I would rather that it still be used in the context of research until formal recommendations can be made by bodies like the NIH and CDC,” Dr. Pillinger said. “But certainly, there may be times when physicians feel compelled to treat patients off label.”

He cautioned, however, that colchicine should never be used with some other drugs. Its interaction with the antibiotic clarithromycin can be fatal, he noted. And, he said, the drug must be monitored in general since it can cause rare, severe problems.

“Overall, colchicine probably works on the overabundant inflammatory response to COVID, and it may be that it can be combined with other drugs that affect viral replication or promote immunity – e.g. vaccines,” Dr. Pillinger said. “So far, it seems as if there is no safety problem with combining colchicine with other approaches, but this has not been studied in a rigorous manner.”

Moving forward, he said, the drug’s very low price outside of the United States “could provide resource-poor countries with a way to help keep patients out of precious hospital beds – or help them go home sooner once admitted.” For now, however, “we need a large-scale inpatient study, and one is currently going on in Great Britain. We also need validation of the outpatient ColCORONA study, and studies to look at whether colchicine can work in conjunction with other strategies.”

The study was funded by grants from the São Paulo Research Foundation, Brazilian National Council for Scientific and Technological Development, and CAPES Foundation. No disclosures are reported. Dr. Pillinger reports serving as an investigator for the ColCORONA trial and receiving a unrelated investigator-initiated grant from Hikma, a colchicine manufacturer.

Despite a drop in the number of weekly COVID-19 cases, children made up a larger share of cases for the fourth consecutive week, according to a report from the American Academy of Pediatrics and the Children’s Hospital Association.

Just over 140,000 new cases of COVID-19 in children were reported for the week of Jan. 22-28, down from 165,000 the week before and down from the record high of 211,000 2 weeks earlier, the AAP and the CHA said in their weekly COVID-19 report.

Since the beginning of January, however, the proportion of weekly cases occurring in children has risen from 12.9% to 15.1%, based on data collected by the AAP/CHA from the health department websites of 49 states (excluding New York), the District of Columbia, New York City, Puerto Rico, and Guam.

Since the beginning of the pandemic, 2.81 million children have been infected by the coronavirus, representing 12.8% of the total for all ages, which is almost 22 million. The cumulative rate since the start of the pandemic passed 3,700 cases per 100,000 children after increasing by 5.2% over the previous week, the AAP and CHA said in their report.

Cumulative hospitalizations in children just passed 11,000 in the 24 states (and New York City) that are reporting data for children, which represents 1.8% of COVID-19–related admissions for all ages, a proportion that has not changed since mid-November. Ten more deaths in children were reported during Jan. 22-28, bringing the total to 215 in the 43 states, along with New York City and Guam, that are tracking mortality.

In the 10 states that are reporting data on testing, rates of positive results in children range from 7.1% in Indiana, in which children make up the largest proportion of total tests performed (18.1%) to 28.4% in Iowa, where children make up the smallest proportion of tests (6.0%), the AAP and CHA said.

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Despite a drop in the number of weekly COVID-19 cases, children made up a larger share of cases for the fourth consecutive week, according to a report from the American Academy of Pediatrics and the Children’s Hospital Association.

Just over 140,000 new cases of COVID-19 in children were reported for the week of Jan. 22-28, down from 165,000 the week before and down from the record high of 211,000 2 weeks earlier, the AAP and the CHA said in their weekly COVID-19 report.

Since the beginning of January, however, the proportion of weekly cases occurring in children has risen from 12.9% to 15.1%, based on data collected by the AAP/CHA from the health department websites of 49 states (excluding New York), the District of Columbia, New York City, Puerto Rico, and Guam.

Since the beginning of the pandemic, 2.81 million children have been infected by the coronavirus, representing 12.8% of the total for all ages, which is almost 22 million. The cumulative rate since the start of the pandemic passed 3,700 cases per 100,000 children after increasing by 5.2% over the previous week, the AAP and CHA said in their report.

Cumulative hospitalizations in children just passed 11,000 in the 24 states (and New York City) that are reporting data for children, which represents 1.8% of COVID-19–related admissions for all ages, a proportion that has not changed since mid-November. Ten more deaths in children were reported during Jan. 22-28, bringing the total to 215 in the 43 states, along with New York City and Guam, that are tracking mortality.

In the 10 states that are reporting data on testing, rates of positive results in children range from 7.1% in Indiana, in which children make up the largest proportion of total tests performed (18.1%) to 28.4% in Iowa, where children make up the smallest proportion of tests (6.0%), the AAP and CHA said.

[email protected]

Despite a drop in the number of weekly COVID-19 cases, children made up a larger share of cases for the fourth consecutive week, according to a report from the American Academy of Pediatrics and the Children’s Hospital Association.

Just over 140,000 new cases of COVID-19 in children were reported for the week of Jan. 22-28, down from 165,000 the week before and down from the record high of 211,000 2 weeks earlier, the AAP and the CHA said in their weekly COVID-19 report.

Since the beginning of January, however, the proportion of weekly cases occurring in children has risen from 12.9% to 15.1%, based on data collected by the AAP/CHA from the health department websites of 49 states (excluding New York), the District of Columbia, New York City, Puerto Rico, and Guam.

Since the beginning of the pandemic, 2.81 million children have been infected by the coronavirus, representing 12.8% of the total for all ages, which is almost 22 million. The cumulative rate since the start of the pandemic passed 3,700 cases per 100,000 children after increasing by 5.2% over the previous week, the AAP and CHA said in their report.

Cumulative hospitalizations in children just passed 11,000 in the 24 states (and New York City) that are reporting data for children, which represents 1.8% of COVID-19–related admissions for all ages, a proportion that has not changed since mid-November. Ten more deaths in children were reported during Jan. 22-28, bringing the total to 215 in the 43 states, along with New York City and Guam, that are tracking mortality.

In the 10 states that are reporting data on testing, rates of positive results in children range from 7.1% in Indiana, in which children make up the largest proportion of total tests performed (18.1%) to 28.4% in Iowa, where children make up the smallest proportion of tests (6.0%), the AAP and CHA said.

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Autopsies on patients who died from COVID-19 are providing important clues on how to treat the disease. In an analysis of 40 hearts from COVID-19 patients who died early in the pandemic, myocyte necrosis was seen in 14 hearts, or 35%.

In the majority of these hearts, pathologists found both small areas of focal necrosis and cardiac thrombi, most of which were microthrombi in myocardial capillaries, arterioles, and small muscular cells.

In an interview, senior author Aloke V. Finn, MD, CVPath Institute, Gaithersburg, Md., stressed the importance of understanding what they saw, but also what they didn’t see.

“What we saw in the majority of patients with myocardial injury were these small areas of infarct and microthrombi in small vessels. What we didn’t see was any evidence of myocarditis and or huge infarcts in, like, the LAD artery,” he said.

“What we’re seeing here is not clinically detectable. ... There is no test that will tell you there are microthrombi and no imaging tests that will show these focal areas of necrosis, but that doesn’t mean it’s not there,” he added.

The finding of myocyte necrosis in about one-third of samples is consistent with another study that showed that 30%-40% of patients hospitalized with COVID-19 have elevated troponins, noted Dr. Finn. The investigators were unable to obtain troponin levels on their patients, which could limit the clinical translation of myocardial necrosis detected at autopsy.

Dr. Finn and colleagues, including first author Dario Pellegrini, MD, from Ospedale Papa Giovanni XXIII in Bergamo, Italy, published their findings online in Circulation on Jan. 22, 2020.

The report is a follow-up to another just published by Dr. Finn’s group in the Journal of the American College of Cardiology, which showed that myocarditis is a very rare finding in COVID-19 autopsies.

Only three of 14 individuals (21.4%) with evidence of myocyte necrosis showed evidence of acute MI, which Dr. Finn and colleagues define as an area of necrosis at least 1 cm² in size. The remaining 11 (78.6%) had only discrete areas of myocyte necrosis (>20 necrotic myocytes with an area of ≥0.05 mm², but <1 cm²).

“This makes sense when we saw what type of thrombus there was in these cases; it wasn’t thrombus in major epicardial vessels but microthombi in small vessels,” said Dr. Finn.

In those with necrosis, cardiac thrombi were present in 11 of 14 (78.6%) cases, with 2 of 14 (14.2%) having epicardial coronary artery thrombi and 0 of 14 (64.3%) having microthrombi in myocardial capillaries, arterioles, and small muscular arteries.

Further supporting the role of COVID-19–related hypercoagulability as the cause of myocardial injury in many patients, the investigators noted that the incidence of severe coronary artery disease (defined as >75% cross sectional narrowing) did not differ significantly between those with and without necrosis.
 

COVID-19 vs. non–COVID-19 thrombi

Going one step further, Dr. Finn’s team compared cardiac microthrombi from their COVID-19–positive autopsy cases with intramyocardial thromboemboli from COVID-19 cases. They also compared the samples with aspirated thrombi obtained during primary percutaneous coronary intervention from uninfected and COVID-19–infected patients presenting with ST-segment elevation MI (STEMI).

The autopsy-obtained microthrombi had significantly more fibrin and terminal complement C5b-9 immunostaining than intramyocardial thromboemboli from COVID-19–negative subjects and than aspirated thrombi from either COVID-positive or COVID-negative STEMI patients.

“Basically, what we’re seeing in these thrombi is evidence of an immune-mediated reaction,” said Dr. Finn, explaining that complement C5b-9 is an innate immune system protein that circulates in the blood in response to any kind of activation of the immune system. “It is nonspecific but can also lead to coagulation problems,” he said.
 

Anticoagulation, yes, but dose unclear

These findings clearly support the use of anticoagulation in hospitalized COVID patients, said Jeffrey Weitz, MD, director of the Thrombosis & Atherosclerosis Research Institute, McMaster University, Hamilton, Ont. But the details of how much anticoagulation, what kind, and for whom are still a moving target.

“I think what we can say at this point is that these autopsy findings fit with previous studies that have shown microthrombi in the lungs and thrombi in the legs and gut, and support the notion that these patients should receive prophylactic doses of anticoagulants if they’re sick enough to be hospitalized,” said Dr. Weitz.

“But it’s not as simple as to say that this study shows clots form in the heart of COVID patients and therefore more anticoagulation is going to be better than less anticoagulation,” he said in an interview.

Recent top-line findings from three linked clinical trials – REMAP-CAP, ACTIV-4, and ATTACC – show that full-dose anticoagulation was beneficial in moderately ill patients hospitalized for COVID-19 and reduced the need for mechanical ventilation.

Moderately ill patients are those not in intensive care and who did not require organ support, such as mechanical ventilation, at the time of enrollment.

However, the same group reported findings in December that showed that routine use of full-dose anticoagulation when started in the ICU in critically ill patients was not beneficial and possibly harmful.

Dr. Weitz was only a little bit surprised by this finding of potential harm in the sickest patients. “I figured everybody should get prophylaxis but I wasn’t sure that everybody should get intensified anticoagulant. But my assumption was that if anybody is going to benefit from it, it would be the ICU patients.”

It was notable, said Dr. Weitz, that levels of D-dimer, a fibrin degradation product, were not associated with outcomes. “So, it doesn’t seem to be that patients with evidence of more clotting are more likely to benefit, which might indicate that it’s not the anticoagulant effect of the heparin that’s helping, but maybe the anti-inflammatory effect. At this point, we just don’t know.”

All three studies have paused enrollment of the critically ill subgroup, but are continuing to enroll patients with moderate illness and expect to publish results in the coming months, according to previous coverage from this news organization.

The study was funded by CVPath, a nonprofit institute that receives funding from a number of different industry entities. Dr. Finn and Dr. Weitz reported no relevant conflicts of interest.

A version of this article first appeared on Medscape.com.

Autopsies on patients who died from COVID-19 are providing important clues on how to treat the disease. In an analysis of 40 hearts from COVID-19 patients who died early in the pandemic, myocyte necrosis was seen in 14 hearts, or 35%.

In the majority of these hearts, pathologists found both small areas of focal necrosis and cardiac thrombi, most of which were microthrombi in myocardial capillaries, arterioles, and small muscular cells.

In an interview, senior author Aloke V. Finn, MD, CVPath Institute, Gaithersburg, Md., stressed the importance of understanding what they saw, but also what they didn’t see.

“What we saw in the majority of patients with myocardial injury were these small areas of infarct and microthrombi in small vessels. What we didn’t see was any evidence of myocarditis and or huge infarcts in, like, the LAD artery,” he said.

“What we’re seeing here is not clinically detectable. ... There is no test that will tell you there are microthrombi and no imaging tests that will show these focal areas of necrosis, but that doesn’t mean it’s not there,” he added.

The finding of myocyte necrosis in about one-third of samples is consistent with another study that showed that 30%-40% of patients hospitalized with COVID-19 have elevated troponins, noted Dr. Finn. The investigators were unable to obtain troponin levels on their patients, which could limit the clinical translation of myocardial necrosis detected at autopsy.

Dr. Finn and colleagues, including first author Dario Pellegrini, MD, from Ospedale Papa Giovanni XXIII in Bergamo, Italy, published their findings online in Circulation on Jan. 22, 2020.

The report is a follow-up to another just published by Dr. Finn’s group in the Journal of the American College of Cardiology, which showed that myocarditis is a very rare finding in COVID-19 autopsies.

Only three of 14 individuals (21.4%) with evidence of myocyte necrosis showed evidence of acute MI, which Dr. Finn and colleagues define as an area of necrosis at least 1 cm² in size. The remaining 11 (78.6%) had only discrete areas of myocyte necrosis (>20 necrotic myocytes with an area of ≥0.05 mm², but <1 cm²).

“This makes sense when we saw what type of thrombus there was in these cases; it wasn’t thrombus in major epicardial vessels but microthombi in small vessels,” said Dr. Finn.

In those with necrosis, cardiac thrombi were present in 11 of 14 (78.6%) cases, with 2 of 14 (14.2%) having epicardial coronary artery thrombi and 0 of 14 (64.3%) having microthrombi in myocardial capillaries, arterioles, and small muscular arteries.

Further supporting the role of COVID-19–related hypercoagulability as the cause of myocardial injury in many patients, the investigators noted that the incidence of severe coronary artery disease (defined as >75% cross sectional narrowing) did not differ significantly between those with and without necrosis.
 

COVID-19 vs. non–COVID-19 thrombi

Going one step further, Dr. Finn’s team compared cardiac microthrombi from their COVID-19–positive autopsy cases with intramyocardial thromboemboli from COVID-19 cases. They also compared the samples with aspirated thrombi obtained during primary percutaneous coronary intervention from uninfected and COVID-19–infected patients presenting with ST-segment elevation MI (STEMI).

The autopsy-obtained microthrombi had significantly more fibrin and terminal complement C5b-9 immunostaining than intramyocardial thromboemboli from COVID-19–negative subjects and than aspirated thrombi from either COVID-positive or COVID-negative STEMI patients.

“Basically, what we’re seeing in these thrombi is evidence of an immune-mediated reaction,” said Dr. Finn, explaining that complement C5b-9 is an innate immune system protein that circulates in the blood in response to any kind of activation of the immune system. “It is nonspecific but can also lead to coagulation problems,” he said.
 

Anticoagulation, yes, but dose unclear

These findings clearly support the use of anticoagulation in hospitalized COVID patients, said Jeffrey Weitz, MD, director of the Thrombosis & Atherosclerosis Research Institute, McMaster University, Hamilton, Ont. But the details of how much anticoagulation, what kind, and for whom are still a moving target.

“I think what we can say at this point is that these autopsy findings fit with previous studies that have shown microthrombi in the lungs and thrombi in the legs and gut, and support the notion that these patients should receive prophylactic doses of anticoagulants if they’re sick enough to be hospitalized,” said Dr. Weitz.

“But it’s not as simple as to say that this study shows clots form in the heart of COVID patients and therefore more anticoagulation is going to be better than less anticoagulation,” he said in an interview.

Recent top-line findings from three linked clinical trials – REMAP-CAP, ACTIV-4, and ATTACC – show that full-dose anticoagulation was beneficial in moderately ill patients hospitalized for COVID-19 and reduced the need for mechanical ventilation.

Moderately ill patients are those not in intensive care and who did not require organ support, such as mechanical ventilation, at the time of enrollment.

However, the same group reported findings in December that showed that routine use of full-dose anticoagulation when started in the ICU in critically ill patients was not beneficial and possibly harmful.

Dr. Weitz was only a little bit surprised by this finding of potential harm in the sickest patients. “I figured everybody should get prophylaxis but I wasn’t sure that everybody should get intensified anticoagulant. But my assumption was that if anybody is going to benefit from it, it would be the ICU patients.”

It was notable, said Dr. Weitz, that levels of D-dimer, a fibrin degradation product, were not associated with outcomes. “So, it doesn’t seem to be that patients with evidence of more clotting are more likely to benefit, which might indicate that it’s not the anticoagulant effect of the heparin that’s helping, but maybe the anti-inflammatory effect. At this point, we just don’t know.”

All three studies have paused enrollment of the critically ill subgroup, but are continuing to enroll patients with moderate illness and expect to publish results in the coming months, according to previous coverage from this news organization.

The study was funded by CVPath, a nonprofit institute that receives funding from a number of different industry entities. Dr. Finn and Dr. Weitz reported no relevant conflicts of interest.

A version of this article first appeared on Medscape.com.

Autopsies on patients who died from COVID-19 are providing important clues on how to treat the disease. In an analysis of 40 hearts from COVID-19 patients who died early in the pandemic, myocyte necrosis was seen in 14 hearts, or 35%.

In the majority of these hearts, pathologists found both small areas of focal necrosis and cardiac thrombi, most of which were microthrombi in myocardial capillaries, arterioles, and small muscular cells.

In an interview, senior author Aloke V. Finn, MD, CVPath Institute, Gaithersburg, Md., stressed the importance of understanding what they saw, but also what they didn’t see.

“What we saw in the majority of patients with myocardial injury were these small areas of infarct and microthrombi in small vessels. What we didn’t see was any evidence of myocarditis and or huge infarcts in, like, the LAD artery,” he said.

“What we’re seeing here is not clinically detectable. ... There is no test that will tell you there are microthrombi and no imaging tests that will show these focal areas of necrosis, but that doesn’t mean it’s not there,” he added.

The finding of myocyte necrosis in about one-third of samples is consistent with another study that showed that 30%-40% of patients hospitalized with COVID-19 have elevated troponins, noted Dr. Finn. The investigators were unable to obtain troponin levels on their patients, which could limit the clinical translation of myocardial necrosis detected at autopsy.

Dr. Finn and colleagues, including first author Dario Pellegrini, MD, from Ospedale Papa Giovanni XXIII in Bergamo, Italy, published their findings online in Circulation on Jan. 22, 2020.

The report is a follow-up to another just published by Dr. Finn’s group in the Journal of the American College of Cardiology, which showed that myocarditis is a very rare finding in COVID-19 autopsies.

Only three of 14 individuals (21.4%) with evidence of myocyte necrosis showed evidence of acute MI, which Dr. Finn and colleagues define as an area of necrosis at least 1 cm² in size. The remaining 11 (78.6%) had only discrete areas of myocyte necrosis (>20 necrotic myocytes with an area of ≥0.05 mm², but <1 cm²).

“This makes sense when we saw what type of thrombus there was in these cases; it wasn’t thrombus in major epicardial vessels but microthombi in small vessels,” said Dr. Finn.

In those with necrosis, cardiac thrombi were present in 11 of 14 (78.6%) cases, with 2 of 14 (14.2%) having epicardial coronary artery thrombi and 0 of 14 (64.3%) having microthrombi in myocardial capillaries, arterioles, and small muscular arteries.

Further supporting the role of COVID-19–related hypercoagulability as the cause of myocardial injury in many patients, the investigators noted that the incidence of severe coronary artery disease (defined as >75% cross sectional narrowing) did not differ significantly between those with and without necrosis.
 

COVID-19 vs. non–COVID-19 thrombi

Going one step further, Dr. Finn’s team compared cardiac microthrombi from their COVID-19–positive autopsy cases with intramyocardial thromboemboli from COVID-19 cases. They also compared the samples with aspirated thrombi obtained during primary percutaneous coronary intervention from uninfected and COVID-19–infected patients presenting with ST-segment elevation MI (STEMI).

The autopsy-obtained microthrombi had significantly more fibrin and terminal complement C5b-9 immunostaining than intramyocardial thromboemboli from COVID-19–negative subjects and than aspirated thrombi from either COVID-positive or COVID-negative STEMI patients.

“Basically, what we’re seeing in these thrombi is evidence of an immune-mediated reaction,” said Dr. Finn, explaining that complement C5b-9 is an innate immune system protein that circulates in the blood in response to any kind of activation of the immune system. “It is nonspecific but can also lead to coagulation problems,” he said.
 

Anticoagulation, yes, but dose unclear

These findings clearly support the use of anticoagulation in hospitalized COVID patients, said Jeffrey Weitz, MD, director of the Thrombosis & Atherosclerosis Research Institute, McMaster University, Hamilton, Ont. But the details of how much anticoagulation, what kind, and for whom are still a moving target.

“I think what we can say at this point is that these autopsy findings fit with previous studies that have shown microthrombi in the lungs and thrombi in the legs and gut, and support the notion that these patients should receive prophylactic doses of anticoagulants if they’re sick enough to be hospitalized,” said Dr. Weitz.

“But it’s not as simple as to say that this study shows clots form in the heart of COVID patients and therefore more anticoagulation is going to be better than less anticoagulation,” he said in an interview.

Recent top-line findings from three linked clinical trials – REMAP-CAP, ACTIV-4, and ATTACC – show that full-dose anticoagulation was beneficial in moderately ill patients hospitalized for COVID-19 and reduced the need for mechanical ventilation.

Moderately ill patients are those not in intensive care and who did not require organ support, such as mechanical ventilation, at the time of enrollment.

However, the same group reported findings in December that showed that routine use of full-dose anticoagulation when started in the ICU in critically ill patients was not beneficial and possibly harmful.

Dr. Weitz was only a little bit surprised by this finding of potential harm in the sickest patients. “I figured everybody should get prophylaxis but I wasn’t sure that everybody should get intensified anticoagulant. But my assumption was that if anybody is going to benefit from it, it would be the ICU patients.”

It was notable, said Dr. Weitz, that levels of D-dimer, a fibrin degradation product, were not associated with outcomes. “So, it doesn’t seem to be that patients with evidence of more clotting are more likely to benefit, which might indicate that it’s not the anticoagulant effect of the heparin that’s helping, but maybe the anti-inflammatory effect. At this point, we just don’t know.”

All three studies have paused enrollment of the critically ill subgroup, but are continuing to enroll patients with moderate illness and expect to publish results in the coming months, according to previous coverage from this news organization.

The study was funded by CVPath, a nonprofit institute that receives funding from a number of different industry entities. Dr. Finn and Dr. Weitz reported no relevant conflicts of interest.

A version of this article first appeared on Medscape.com.

The Janssen/Johnson & Johnson single-dose adenovirus vaccine provides 85% efficacy globally against severe COVID-19 illness, according to the highly anticipated interim phase 3 results announced this morning.

The efficacy against severe disease provided by the Janssen/J&J vaccine held true regardless of age, race/ethnicity, absence or presence of comorbidities, and geography. The 44,000-participant ENSEMBLE study was conducted in the United States, South America, and South Africa.

“The team is very diligently monitoring all the variants that come up, and there are literally thousands of these. We are acting in anticipation of a variant being a potential problem. The South African variant we too acted on right away. So we too are preparing that antigen for testing.

“With data today, we do see that not a single South African, after 28 days post vaccination, ended up needing to go to the hospital, no South African died who was vaccinated.

“We do see that 85%-plus protection in South African against severe disease. That is one of the most exciting results in the dataset today,” said Mathai Mammen, MD, PhD, global head of Janssen Research & Development.

The overall efficacy was 66% globally, 72% in the United States, 66% in Latin America, and 57% in South Africa against moderate to severe SARS-CoV-2 28 days post vaccination, officials from the National Institutes of Health and Janssen reported during a media briefing.

But the J&J vaccine has potential advantages over the existing two-dose Pfizer/BioNTech and Moderna mRNA vaccines because it’s single dose and has less stringent storage requirements – only regular refrigeration is needed versus a need to freeze the two-dose Pfizer/BioNTech and Moderna COVID-19 vaccines. The J&J vaccine can be refrigerated for up to 3 months at 36°-46° F (2°-8° C).

But the difference between these just-released efficacy figures and the 94%-95% efficacy provided by the existing Pfizer/BioNTech and Moderna mRNA vaccines generated many questions during the briefing.

Anthony Fauci, MD, director of the National Institute of Allergy and Infectious Diseases, said the focus should not just be on the overall numbers. “The most important thing from a public health standpoint domestically is to keep people out of the hospital and prevent them from getting severe illness,” he said. “Many in the general public might look at a number and want to know if they get symptomatic disease or not.”

“More important than preventing someone from getting some aches and a sore throat is to prevent people – particularly people who have underlying conditions and the elderly, the ones most susceptible to a severe outcome – [from getting] severe disease,” Dr. Fauci added. Prevention of severe outcomes in a high percentage of individuals “will alleviate so much of the stress, human suffering, and death.”

Dr. Fauci acknowledged that many people will naturally focus on the distinction between 72% efficacy and 94%-95% efficacy. “This could be a messaging challenge [but] you have to make sure people understand the implications.”

It is more complex, he added, than just asking people: “If you go to the door on the left, you get 94% or 95%. If you go to the door to the right, you get 72%. What door do you want to go to?”

Instead, the messaging should be that “this and the other vaccines we have are actually preventing severe disease to a very substantial degree.”
 

Company defends numbers

Janssen defended their efficacy findings, pointing out that it is not a fair comparison.

“The vaccine programs that went a couple of months ago, they ran their studies during different times, when the pandemic was less complex. There were not these variants, and there was not the same level of incidence, which puts pressure on vaccine efficacy,” said Mathai Mammen, MD, PhD, global head of research and development for Janssen.

“So the numbers cannot really be compared, and that does pose a messaging challenge,” he said. “But the reality is, if one was to run the same studies [for the Pfizer and Moderna vaccines] today you would likely see different results.”

Asked if the efficacy figures could affect vaccine hesitancy, National Institutes of Health Director Francis Collins, MD, PhD, said at the announcement that most reluctance among people to get vaccinated against SARS-CoV-2 stems from concerns about safety. “The safety record is extremely good for this vaccine, as it is for the others that have received emergency use authorization.”

Janssen/J&J plans to submit for emergency use authorization from the U.S. Food and Drug Administration next week, at which point the company plans to release more information on side effects, deaths, and patient subpopulation efficacy, and more from the ENSEMBLE trial.

Janssen is aiming to provide 1 billion doses by the end of this year.

A version of this article first appeared on Medscape.com.

The Janssen/Johnson & Johnson single-dose adenovirus vaccine provides 85% efficacy globally against severe COVID-19 illness, according to the highly anticipated interim phase 3 results announced this morning.

The efficacy against severe disease provided by the Janssen/J&J vaccine held true regardless of age, race/ethnicity, absence or presence of comorbidities, and geography. The 44,000-participant ENSEMBLE study was conducted in the United States, South America, and South Africa.

“The team is very diligently monitoring all the variants that come up, and there are literally thousands of these. We are acting in anticipation of a variant being a potential problem. The South African variant we too acted on right away. So we too are preparing that antigen for testing.

“With data today, we do see that not a single South African, after 28 days post vaccination, ended up needing to go to the hospital, no South African died who was vaccinated.

“We do see that 85%-plus protection in South African against severe disease. That is one of the most exciting results in the dataset today,” said Mathai Mammen, MD, PhD, global head of Janssen Research & Development.

The overall efficacy was 66% globally, 72% in the United States, 66% in Latin America, and 57% in South Africa against moderate to severe SARS-CoV-2 28 days post vaccination, officials from the National Institutes of Health and Janssen reported during a media briefing.

But the J&J vaccine has potential advantages over the existing two-dose Pfizer/BioNTech and Moderna mRNA vaccines because it’s single dose and has less stringent storage requirements – only regular refrigeration is needed versus a need to freeze the two-dose Pfizer/BioNTech and Moderna COVID-19 vaccines. The J&J vaccine can be refrigerated for up to 3 months at 36°-46° F (2°-8° C).

But the difference between these just-released efficacy figures and the 94%-95% efficacy provided by the existing Pfizer/BioNTech and Moderna mRNA vaccines generated many questions during the briefing.

Anthony Fauci, MD, director of the National Institute of Allergy and Infectious Diseases, said the focus should not just be on the overall numbers. “The most important thing from a public health standpoint domestically is to keep people out of the hospital and prevent them from getting severe illness,” he said. “Many in the general public might look at a number and want to know if they get symptomatic disease or not.”

“More important than preventing someone from getting some aches and a sore throat is to prevent people – particularly people who have underlying conditions and the elderly, the ones most susceptible to a severe outcome – [from getting] severe disease,” Dr. Fauci added. Prevention of severe outcomes in a high percentage of individuals “will alleviate so much of the stress, human suffering, and death.”

Dr. Fauci acknowledged that many people will naturally focus on the distinction between 72% efficacy and 94%-95% efficacy. “This could be a messaging challenge [but] you have to make sure people understand the implications.”

It is more complex, he added, than just asking people: “If you go to the door on the left, you get 94% or 95%. If you go to the door to the right, you get 72%. What door do you want to go to?”

Instead, the messaging should be that “this and the other vaccines we have are actually preventing severe disease to a very substantial degree.”
 

Company defends numbers

Janssen defended their efficacy findings, pointing out that it is not a fair comparison.

“The vaccine programs that went a couple of months ago, they ran their studies during different times, when the pandemic was less complex. There were not these variants, and there was not the same level of incidence, which puts pressure on vaccine efficacy,” said Mathai Mammen, MD, PhD, global head of research and development for Janssen.

“So the numbers cannot really be compared, and that does pose a messaging challenge,” he said. “But the reality is, if one was to run the same studies [for the Pfizer and Moderna vaccines] today you would likely see different results.”

Asked if the efficacy figures could affect vaccine hesitancy, National Institutes of Health Director Francis Collins, MD, PhD, said at the announcement that most reluctance among people to get vaccinated against SARS-CoV-2 stems from concerns about safety. “The safety record is extremely good for this vaccine, as it is for the others that have received emergency use authorization.”

Janssen/J&J plans to submit for emergency use authorization from the U.S. Food and Drug Administration next week, at which point the company plans to release more information on side effects, deaths, and patient subpopulation efficacy, and more from the ENSEMBLE trial.

Janssen is aiming to provide 1 billion doses by the end of this year.

A version of this article first appeared on Medscape.com.

The Janssen/Johnson & Johnson single-dose adenovirus vaccine provides 85% efficacy globally against severe COVID-19 illness, according to the highly anticipated interim phase 3 results announced this morning.

The efficacy against severe disease provided by the Janssen/J&J vaccine held true regardless of age, race/ethnicity, absence or presence of comorbidities, and geography. The 44,000-participant ENSEMBLE study was conducted in the United States, South America, and South Africa.

“The team is very diligently monitoring all the variants that come up, and there are literally thousands of these. We are acting in anticipation of a variant being a potential problem. The South African variant we too acted on right away. So we too are preparing that antigen for testing.

“With data today, we do see that not a single South African, after 28 days post vaccination, ended up needing to go to the hospital, no South African died who was vaccinated.

“We do see that 85%-plus protection in South African against severe disease. That is one of the most exciting results in the dataset today,” said Mathai Mammen, MD, PhD, global head of Janssen Research & Development.

The overall efficacy was 66% globally, 72% in the United States, 66% in Latin America, and 57% in South Africa against moderate to severe SARS-CoV-2 28 days post vaccination, officials from the National Institutes of Health and Janssen reported during a media briefing.

But the J&J vaccine has potential advantages over the existing two-dose Pfizer/BioNTech and Moderna mRNA vaccines because it’s single dose and has less stringent storage requirements – only regular refrigeration is needed versus a need to freeze the two-dose Pfizer/BioNTech and Moderna COVID-19 vaccines. The J&J vaccine can be refrigerated for up to 3 months at 36°-46° F (2°-8° C).

But the difference between these just-released efficacy figures and the 94%-95% efficacy provided by the existing Pfizer/BioNTech and Moderna mRNA vaccines generated many questions during the briefing.

Anthony Fauci, MD, director of the National Institute of Allergy and Infectious Diseases, said the focus should not just be on the overall numbers. “The most important thing from a public health standpoint domestically is to keep people out of the hospital and prevent them from getting severe illness,” he said. “Many in the general public might look at a number and want to know if they get symptomatic disease or not.”

“More important than preventing someone from getting some aches and a sore throat is to prevent people – particularly people who have underlying conditions and the elderly, the ones most susceptible to a severe outcome – [from getting] severe disease,” Dr. Fauci added. Prevention of severe outcomes in a high percentage of individuals “will alleviate so much of the stress, human suffering, and death.”

Dr. Fauci acknowledged that many people will naturally focus on the distinction between 72% efficacy and 94%-95% efficacy. “This could be a messaging challenge [but] you have to make sure people understand the implications.”

It is more complex, he added, than just asking people: “If you go to the door on the left, you get 94% or 95%. If you go to the door to the right, you get 72%. What door do you want to go to?”

Instead, the messaging should be that “this and the other vaccines we have are actually preventing severe disease to a very substantial degree.”
 

Company defends numbers

Janssen defended their efficacy findings, pointing out that it is not a fair comparison.

“The vaccine programs that went a couple of months ago, they ran their studies during different times, when the pandemic was less complex. There were not these variants, and there was not the same level of incidence, which puts pressure on vaccine efficacy,” said Mathai Mammen, MD, PhD, global head of research and development for Janssen.

“So the numbers cannot really be compared, and that does pose a messaging challenge,” he said. “But the reality is, if one was to run the same studies [for the Pfizer and Moderna vaccines] today you would likely see different results.”

Asked if the efficacy figures could affect vaccine hesitancy, National Institutes of Health Director Francis Collins, MD, PhD, said at the announcement that most reluctance among people to get vaccinated against SARS-CoV-2 stems from concerns about safety. “The safety record is extremely good for this vaccine, as it is for the others that have received emergency use authorization.”

Janssen/J&J plans to submit for emergency use authorization from the U.S. Food and Drug Administration next week, at which point the company plans to release more information on side effects, deaths, and patient subpopulation efficacy, and more from the ENSEMBLE trial.

Janssen is aiming to provide 1 billion doses by the end of this year.

A version of this article first appeared on Medscape.com.

The United States is facing a “Category 5” storm as coronavirus variants begin to spread across the country, one of the nation’s top infectious disease experts said Sunday.

“We are going to see something like we have not seen yet in this country,” Michael Osterholm, PhD, MPH, director of the Center for Infectious Disease Research and Policy at the University of Minnesota, Minneapolis, said on NBC’s Meet the Press.

The United States has reported 467 cases of the coronavirus variant first identified in the United Kingdom, across 32 states, according to the CDC variant tracker. The United States has also reported three cases of the variant first identified in South Africa in South Carolina and Maryland. One case of the variant first identified in Brazil has been found in Minnesota.

Although overall COVID-19 cases and hospitalizations have declined during the past few weeks, another storm is brewing on the horizon with the variants, Dr. Osterholm told host Chuck Todd. The U.K. variant will likely cause a surge in COVID-19 cases during the next 6-14 weeks, he said. “You and I are sitting on this beach where it’s 70 degrees, perfectly blue skies, gentle breeze. But I see that hurricane 5, Category 5 or higher, 450 miles offshore. And telling people to evacuate on that nice blue sky day is going to be hard. But I can also tell you that hurricane is coming.”

Dr. Osterholm urged federal and state officials to vaccinate as many people as possible to reduce the oncoming storm. The United States has distributed 49.9 million doses and administered 31.1 million doses, according to the latest CDC data updated Sunday, including 25.2 million first doses and 5.6 million second doses.

Doling out more doses to older Americans, rather than holding onto the second dose of the two-shot regimen, is an urgent decision, Dr. Osterholm said.

“I think right now, in advance of this surge, we need to get as many one doses in as many people over 65 as we possibly can to reduce serious illnesses and deaths that are going to occur over the weeks ahead,” he said.

The U.K. variant will likely become the dominant coronavirus strain in the United States in coming weeks, Dr. Osterholm said, adding that COVID-19 vaccines should be able to protect against it. In the meantime, however, he’s worried that the variant will cause more infections and deaths until more people get vaccinated.

“What we have to do now is also anticipate this and understand that we’re going to have change quickly,” he said. “As fast as we’re opening restaurants, we’re likely going to be closing them in the near term.”

A version of this article first appeared on WebMD.com.

The United States is facing a “Category 5” storm as coronavirus variants begin to spread across the country, one of the nation’s top infectious disease experts said Sunday.

“We are going to see something like we have not seen yet in this country,” Michael Osterholm, PhD, MPH, director of the Center for Infectious Disease Research and Policy at the University of Minnesota, Minneapolis, said on NBC’s Meet the Press.

The United States has reported 467 cases of the coronavirus variant first identified in the United Kingdom, across 32 states, according to the CDC variant tracker. The United States has also reported three cases of the variant first identified in South Africa in South Carolina and Maryland. One case of the variant first identified in Brazil has been found in Minnesota.

Although overall COVID-19 cases and hospitalizations have declined during the past few weeks, another storm is brewing on the horizon with the variants, Dr. Osterholm told host Chuck Todd. The U.K. variant will likely cause a surge in COVID-19 cases during the next 6-14 weeks, he said. “You and I are sitting on this beach where it’s 70 degrees, perfectly blue skies, gentle breeze. But I see that hurricane 5, Category 5 or higher, 450 miles offshore. And telling people to evacuate on that nice blue sky day is going to be hard. But I can also tell you that hurricane is coming.”

Dr. Osterholm urged federal and state officials to vaccinate as many people as possible to reduce the oncoming storm. The United States has distributed 49.9 million doses and administered 31.1 million doses, according to the latest CDC data updated Sunday, including 25.2 million first doses and 5.6 million second doses.

Doling out more doses to older Americans, rather than holding onto the second dose of the two-shot regimen, is an urgent decision, Dr. Osterholm said.

“I think right now, in advance of this surge, we need to get as many one doses in as many people over 65 as we possibly can to reduce serious illnesses and deaths that are going to occur over the weeks ahead,” he said.

The U.K. variant will likely become the dominant coronavirus strain in the United States in coming weeks, Dr. Osterholm said, adding that COVID-19 vaccines should be able to protect against it. In the meantime, however, he’s worried that the variant will cause more infections and deaths until more people get vaccinated.

“What we have to do now is also anticipate this and understand that we’re going to have change quickly,” he said. “As fast as we’re opening restaurants, we’re likely going to be closing them in the near term.”

A version of this article first appeared on WebMD.com.

The United States is facing a “Category 5” storm as coronavirus variants begin to spread across the country, one of the nation’s top infectious disease experts said Sunday.

“We are going to see something like we have not seen yet in this country,” Michael Osterholm, PhD, MPH, director of the Center for Infectious Disease Research and Policy at the University of Minnesota, Minneapolis, said on NBC’s Meet the Press.

The United States has reported 467 cases of the coronavirus variant first identified in the United Kingdom, across 32 states, according to the CDC variant tracker. The United States has also reported three cases of the variant first identified in South Africa in South Carolina and Maryland. One case of the variant first identified in Brazil has been found in Minnesota.

Although overall COVID-19 cases and hospitalizations have declined during the past few weeks, another storm is brewing on the horizon with the variants, Dr. Osterholm told host Chuck Todd. The U.K. variant will likely cause a surge in COVID-19 cases during the next 6-14 weeks, he said. “You and I are sitting on this beach where it’s 70 degrees, perfectly blue skies, gentle breeze. But I see that hurricane 5, Category 5 or higher, 450 miles offshore. And telling people to evacuate on that nice blue sky day is going to be hard. But I can also tell you that hurricane is coming.”

Dr. Osterholm urged federal and state officials to vaccinate as many people as possible to reduce the oncoming storm. The United States has distributed 49.9 million doses and administered 31.1 million doses, according to the latest CDC data updated Sunday, including 25.2 million first doses and 5.6 million second doses.

Doling out more doses to older Americans, rather than holding onto the second dose of the two-shot regimen, is an urgent decision, Dr. Osterholm said.

“I think right now, in advance of this surge, we need to get as many one doses in as many people over 65 as we possibly can to reduce serious illnesses and deaths that are going to occur over the weeks ahead,” he said.

The U.K. variant will likely become the dominant coronavirus strain in the United States in coming weeks, Dr. Osterholm said, adding that COVID-19 vaccines should be able to protect against it. In the meantime, however, he’s worried that the variant will cause more infections and deaths until more people get vaccinated.

“What we have to do now is also anticipate this and understand that we’re going to have change quickly,” he said. “As fast as we’re opening restaurants, we’re likely going to be closing them in the near term.”

A version of this article first appeared on WebMD.com.

More people with fever and body aches are turning to NSAIDs to ease symptoms, but the drugs have come under new scrutiny as investigators work to determine whether they are a safe way to relieve the pain of COVID-19 vaccination or symptoms of the disease.

Early on in the pandemic, French health officials warned that NSAIDs, such as ibuprofen, could worsen coronavirus disease, and they recommended switching to acetaminophen instead.

The National Health Service in the United Kingdom followed with a similar recommendation for acetaminophen.

But the European Medicines Agency took a different approach, reporting “no scientific evidence” that NSAIDs could worsen COVID-19. The U.S. Food and Drug Administration also opted not to take a stance.

The debate prompted discussion on social media, with various reactions from around the world. It also inspired Craig Wilen, MD, PhD, from Yale University, New Haven, Conn., and associates to examine the effect of NSAIDs on COVID-19 infection and immune response. Their findings were published online Jan.20 in the Journal of Virology.

“It really bothered me that non–evidence-based decisions were driving the conversation,” Dr. Wilen said. “Millions of people are taking NSAIDs every day and clinical decisions about their care shouldn’t be made on a hypothesis.”

One theory is that NSAIDs alter susceptibility to infection by modifying ACE2. The drugs might also change the cell entry receptor for SARS-CoV-2, alter virus replication, or even modify the immune response.

British researchers, also questioning the safety of NSAIDs in patients with COVID-19, delved into National Health Service records to study two large groups of patients, some of whom were taking the pain relievers.

“We were watching the controversy and the lack of evidence and wanted to contribute,” lead investigator Angel Wong, PhD, from the London School of Hygiene and Tropical Medicine, said in an interview.

And with nearly 11 million NSAID prescriptions dispensed in primary care in England alone in the past 12 months, the inconsistency was concerning.

The team compared COVID-19–related deaths in two groups: one group of more than 700,000 people taking NSAIDs, including patients with rheumatoid arthritis and osteoarthritis; and another of almost 3.5 million people not on the medication.

NSAIDs work by inhibiting cyclooxygenase-1 and COX-2 enzymes in the body, which are crucial for the generation of prostaglandins. These lipid molecules play a role in inflammation and are blocked by NSAIDs.

The investigators found no evidence of a harmful effect of NSAIDs on COVID-19-related deaths; their results were published online Jan. 21 in the Annals of the Rheumatic Diseases.

The results, they pointed out, are in line with a Danish study that also showed no evidence of a higher risk for severe COVID-19 outcomes with NSAID use.

“It’s reassuring,” Dr. Wong said, “that patients can safely continue treatment.”
 

More new evidence

Dr. Wilen’s team found that SARS-CoV-2 infection stimulated COX-2 expression in human and mice cells. However, suppression of COX-2 by two commonly used NSAIDs, ibuprofen and meloxicam, had no effect on ACE2 expression, viral entry, or viral replication.

In their mouse model of SARS-CoV-2 infection, the investigators saw that NSAIDs impaired the production of proinflammatory cytokines and neutralizing antibodies. The findings suggest that NSAIDs influence COVID-19 outcomes by dampening the inflammatory response and production of protective antibodies, rather than modifying susceptibility to infection or viral replication.

Understanding the effect of NSAIDs on cytokine production is critical, Dr. Wilen pointed out, because they might be protective early in COVID-19 but pathologic at later stages.

Timing is crucial in the case of other immunomodulatory drugs. For example, dexamethasone lowers mortality in COVID-19 patients on respiratory support but is potentially harmful for those with milder disease.

There still is a lot to learn, Dr. Wilen acknowledged. “We may be seeing something similar going on with NSAIDs, where the timing of treatment is important.”

A version of this article first appeared on Medscape.com.

More people with fever and body aches are turning to NSAIDs to ease symptoms, but the drugs have come under new scrutiny as investigators work to determine whether they are a safe way to relieve the pain of COVID-19 vaccination or symptoms of the disease.

Early on in the pandemic, French health officials warned that NSAIDs, such as ibuprofen, could worsen coronavirus disease, and they recommended switching to acetaminophen instead.

The National Health Service in the United Kingdom followed with a similar recommendation for acetaminophen.

But the European Medicines Agency took a different approach, reporting “no scientific evidence” that NSAIDs could worsen COVID-19. The U.S. Food and Drug Administration also opted not to take a stance.

The debate prompted discussion on social media, with various reactions from around the world. It also inspired Craig Wilen, MD, PhD, from Yale University, New Haven, Conn., and associates to examine the effect of NSAIDs on COVID-19 infection and immune response. Their findings were published online Jan.20 in the Journal of Virology.

“It really bothered me that non–evidence-based decisions were driving the conversation,” Dr. Wilen said. “Millions of people are taking NSAIDs every day and clinical decisions about their care shouldn’t be made on a hypothesis.”

One theory is that NSAIDs alter susceptibility to infection by modifying ACE2. The drugs might also change the cell entry receptor for SARS-CoV-2, alter virus replication, or even modify the immune response.

British researchers, also questioning the safety of NSAIDs in patients with COVID-19, delved into National Health Service records to study two large groups of patients, some of whom were taking the pain relievers.

“We were watching the controversy and the lack of evidence and wanted to contribute,” lead investigator Angel Wong, PhD, from the London School of Hygiene and Tropical Medicine, said in an interview.

And with nearly 11 million NSAID prescriptions dispensed in primary care in England alone in the past 12 months, the inconsistency was concerning.

The team compared COVID-19–related deaths in two groups: one group of more than 700,000 people taking NSAIDs, including patients with rheumatoid arthritis and osteoarthritis; and another of almost 3.5 million people not on the medication.

NSAIDs work by inhibiting cyclooxygenase-1 and COX-2 enzymes in the body, which are crucial for the generation of prostaglandins. These lipid molecules play a role in inflammation and are blocked by NSAIDs.

The investigators found no evidence of a harmful effect of NSAIDs on COVID-19-related deaths; their results were published online Jan. 21 in the Annals of the Rheumatic Diseases.

The results, they pointed out, are in line with a Danish study that also showed no evidence of a higher risk for severe COVID-19 outcomes with NSAID use.

“It’s reassuring,” Dr. Wong said, “that patients can safely continue treatment.”
 

More new evidence

Dr. Wilen’s team found that SARS-CoV-2 infection stimulated COX-2 expression in human and mice cells. However, suppression of COX-2 by two commonly used NSAIDs, ibuprofen and meloxicam, had no effect on ACE2 expression, viral entry, or viral replication.

In their mouse model of SARS-CoV-2 infection, the investigators saw that NSAIDs impaired the production of proinflammatory cytokines and neutralizing antibodies. The findings suggest that NSAIDs influence COVID-19 outcomes by dampening the inflammatory response and production of protective antibodies, rather than modifying susceptibility to infection or viral replication.

Understanding the effect of NSAIDs on cytokine production is critical, Dr. Wilen pointed out, because they might be protective early in COVID-19 but pathologic at later stages.

Timing is crucial in the case of other immunomodulatory drugs. For example, dexamethasone lowers mortality in COVID-19 patients on respiratory support but is potentially harmful for those with milder disease.

There still is a lot to learn, Dr. Wilen acknowledged. “We may be seeing something similar going on with NSAIDs, where the timing of treatment is important.”

A version of this article first appeared on Medscape.com.

More people with fever and body aches are turning to NSAIDs to ease symptoms, but the drugs have come under new scrutiny as investigators work to determine whether they are a safe way to relieve the pain of COVID-19 vaccination or symptoms of the disease.

Early on in the pandemic, French health officials warned that NSAIDs, such as ibuprofen, could worsen coronavirus disease, and they recommended switching to acetaminophen instead.

The National Health Service in the United Kingdom followed with a similar recommendation for acetaminophen.

But the European Medicines Agency took a different approach, reporting “no scientific evidence” that NSAIDs could worsen COVID-19. The U.S. Food and Drug Administration also opted not to take a stance.

The debate prompted discussion on social media, with various reactions from around the world. It also inspired Craig Wilen, MD, PhD, from Yale University, New Haven, Conn., and associates to examine the effect of NSAIDs on COVID-19 infection and immune response. Their findings were published online Jan.20 in the Journal of Virology.

“It really bothered me that non–evidence-based decisions were driving the conversation,” Dr. Wilen said. “Millions of people are taking NSAIDs every day and clinical decisions about their care shouldn’t be made on a hypothesis.”

One theory is that NSAIDs alter susceptibility to infection by modifying ACE2. The drugs might also change the cell entry receptor for SARS-CoV-2, alter virus replication, or even modify the immune response.

British researchers, also questioning the safety of NSAIDs in patients with COVID-19, delved into National Health Service records to study two large groups of patients, some of whom were taking the pain relievers.

“We were watching the controversy and the lack of evidence and wanted to contribute,” lead investigator Angel Wong, PhD, from the London School of Hygiene and Tropical Medicine, said in an interview.

And with nearly 11 million NSAID prescriptions dispensed in primary care in England alone in the past 12 months, the inconsistency was concerning.

The team compared COVID-19–related deaths in two groups: one group of more than 700,000 people taking NSAIDs, including patients with rheumatoid arthritis and osteoarthritis; and another of almost 3.5 million people not on the medication.

NSAIDs work by inhibiting cyclooxygenase-1 and COX-2 enzymes in the body, which are crucial for the generation of prostaglandins. These lipid molecules play a role in inflammation and are blocked by NSAIDs.

The investigators found no evidence of a harmful effect of NSAIDs on COVID-19-related deaths; their results were published online Jan. 21 in the Annals of the Rheumatic Diseases.

The results, they pointed out, are in line with a Danish study that also showed no evidence of a higher risk for severe COVID-19 outcomes with NSAID use.

“It’s reassuring,” Dr. Wong said, “that patients can safely continue treatment.”
 

More new evidence

Dr. Wilen’s team found that SARS-CoV-2 infection stimulated COX-2 expression in human and mice cells. However, suppression of COX-2 by two commonly used NSAIDs, ibuprofen and meloxicam, had no effect on ACE2 expression, viral entry, or viral replication.

In their mouse model of SARS-CoV-2 infection, the investigators saw that NSAIDs impaired the production of proinflammatory cytokines and neutralizing antibodies. The findings suggest that NSAIDs influence COVID-19 outcomes by dampening the inflammatory response and production of protective antibodies, rather than modifying susceptibility to infection or viral replication.

Understanding the effect of NSAIDs on cytokine production is critical, Dr. Wilen pointed out, because they might be protective early in COVID-19 but pathologic at later stages.

Timing is crucial in the case of other immunomodulatory drugs. For example, dexamethasone lowers mortality in COVID-19 patients on respiratory support but is potentially harmful for those with milder disease.

There still is a lot to learn, Dr. Wilen acknowledged. “We may be seeing something similar going on with NSAIDs, where the timing of treatment is important.”

A version of this article first appeared on Medscape.com.

New data on COVID-19 vaccines should serve as a “wake-up call” about the need to stop the spread of the SARS-CoV-2 virus among people and thus deprive it of opportunities to evolve its defenses, the top federal expert on infectious diseases said.

“The virus will continue to mutate and will mutate for its own selective advantage,” said Anthony S. Fauci, MD, director of the National Institute of Allergy and Infectious Diseases, at a Friday news conference organized by the White House.

The continued transmission of SARS-CoV-2 “gives the virus the chance to adapt to the forces, in this case the immune response, that’s trying to get rid of it,” Dr. Fauci said. “That’s where you get mutations.”

Federal health officials are working to boost the U.S. supply of COVID-19 vaccines, even as signals emerge about the extent that the virus is already evolving.

Data released this week about the Janssen/Johnson & Johnson (J&J) and Novavax COVID-19 vaccines in late-stage development provides further evidence that they may not protect as well against emerging variants, Dr. Fauci said.

“Mutations that lead to different lineage do have clinical consequences,” he said, while also emphasizing that the emerging vaccines appear to confer broad protection. Dr. Fauci earlier in the day addressed the “messaging challenge” for clinicians and researchers in discussing the results of the J&J vaccine trial, which appear to fall short of those reported for the two vaccines already approved and in use in the United States. He noted the benefits of possibly soon having more authorized vaccines to combat COVID-19. But continued community spread of the infection will foster conditions that can undermine the vaccines’ effectiveness.

“Even though the long-range effect in the sense of severe disease is still handled reasonably well by the vaccines, this is a wake-up call to all of us,” Dr. Fauci said.

Pharmaceutical scientists and executives and government health officials will need to work together to continue to develop vaccines that can outwit the emerging variants, he said.

On Jan. 29, J&J reported that its highly anticipated single-dose vaccine had shown its worst results in South Africa where many cases of COVID-19 were caused by infection with a SARS-CoV-2 variant from the B.1.351 lineage. The overall efficacy was 66% globally, 72% in the United States, and 57% in South Africa against moderate to severe SARS-CoV-2, J&J said.

Novavax on Jan. 28 reported an efficacy rate for its COVID-19 vaccine of 49.4% from a clinical trial conducted in South Africa, compared with an 89.3% rate from a U.K. study. There already have been attempts to estimate how well the Pfizer/BioNTech and Moderna vaccines can handle new variants of the virus. They both have been granted emergency-use authorization by the U.S. Food and Drug Administration.
 

‘Genomic surveillance’

The Centers for Disease Control and Prevention on Thursday reported the first U.S.-documented cases of the B.1.351 variant of SARS-CoV-2 in South Carolina. On Jan. 26, the first confirmed U.S. case of a highly transmissible Brazilian coronavirus variant was detected in Minnesota, state health officials said.

The CDC’s stepped-up “genomic surveillance” will help keep clinicians and researchers aware of how SARS-CoV-2 is changing, Dr. Fauci said.

Speaking at the same White House news conference, CDC director Rochelle Walensky, MD, MPH, said the two South Carolina cases of the B.1.351 variant were reported in different parts of the state and not believed to be epidemiologically linked. The people involved “did not have any travel history,” she added.

The SARS-CoV-2 mutations were expected to emerge at some point, as with any virus, but their appearance underscores the need for people to remain vigilant about precautions that can stop its spread, Dr. Walensky said.

She and Dr. Fauci both stressed the need for continued use of masks and social distancing and urged people to get COVID-19 vaccines as they become available. Continued community spread of the virus allows this global health threat to keep replicating, and thus increases its chances to thwart medical interventions, Dr. Fauci said.

“The virus has a playing field, as it were, to mutate,” Dr. Fauci said. “If you stop that and stop the replication, the viruses cannot mutate if they don’t replicate.”

A version of this article first appeared on Medscape.com.

New data on COVID-19 vaccines should serve as a “wake-up call” about the need to stop the spread of the SARS-CoV-2 virus among people and thus deprive it of opportunities to evolve its defenses, the top federal expert on infectious diseases said.

“The virus will continue to mutate and will mutate for its own selective advantage,” said Anthony S. Fauci, MD, director of the National Institute of Allergy and Infectious Diseases, at a Friday news conference organized by the White House.

The continued transmission of SARS-CoV-2 “gives the virus the chance to adapt to the forces, in this case the immune response, that’s trying to get rid of it,” Dr. Fauci said. “That’s where you get mutations.”

Federal health officials are working to boost the U.S. supply of COVID-19 vaccines, even as signals emerge about the extent that the virus is already evolving.

Data released this week about the Janssen/Johnson & Johnson (J&J) and Novavax COVID-19 vaccines in late-stage development provides further evidence that they may not protect as well against emerging variants, Dr. Fauci said.

“Mutations that lead to different lineage do have clinical consequences,” he said, while also emphasizing that the emerging vaccines appear to confer broad protection. Dr. Fauci earlier in the day addressed the “messaging challenge” for clinicians and researchers in discussing the results of the J&J vaccine trial, which appear to fall short of those reported for the two vaccines already approved and in use in the United States. He noted the benefits of possibly soon having more authorized vaccines to combat COVID-19. But continued community spread of the infection will foster conditions that can undermine the vaccines’ effectiveness.

“Even though the long-range effect in the sense of severe disease is still handled reasonably well by the vaccines, this is a wake-up call to all of us,” Dr. Fauci said.

Pharmaceutical scientists and executives and government health officials will need to work together to continue to develop vaccines that can outwit the emerging variants, he said.

On Jan. 29, J&J reported that its highly anticipated single-dose vaccine had shown its worst results in South Africa where many cases of COVID-19 were caused by infection with a SARS-CoV-2 variant from the B.1.351 lineage. The overall efficacy was 66% globally, 72% in the United States, and 57% in South Africa against moderate to severe SARS-CoV-2, J&J said.

Novavax on Jan. 28 reported an efficacy rate for its COVID-19 vaccine of 49.4% from a clinical trial conducted in South Africa, compared with an 89.3% rate from a U.K. study. There already have been attempts to estimate how well the Pfizer/BioNTech and Moderna vaccines can handle new variants of the virus. They both have been granted emergency-use authorization by the U.S. Food and Drug Administration.
 

‘Genomic surveillance’

The Centers for Disease Control and Prevention on Thursday reported the first U.S.-documented cases of the B.1.351 variant of SARS-CoV-2 in South Carolina. On Jan. 26, the first confirmed U.S. case of a highly transmissible Brazilian coronavirus variant was detected in Minnesota, state health officials said.

The CDC’s stepped-up “genomic surveillance” will help keep clinicians and researchers aware of how SARS-CoV-2 is changing, Dr. Fauci said.

Speaking at the same White House news conference, CDC director Rochelle Walensky, MD, MPH, said the two South Carolina cases of the B.1.351 variant were reported in different parts of the state and not believed to be epidemiologically linked. The people involved “did not have any travel history,” she added.

The SARS-CoV-2 mutations were expected to emerge at some point, as with any virus, but their appearance underscores the need for people to remain vigilant about precautions that can stop its spread, Dr. Walensky said.

She and Dr. Fauci both stressed the need for continued use of masks and social distancing and urged people to get COVID-19 vaccines as they become available. Continued community spread of the virus allows this global health threat to keep replicating, and thus increases its chances to thwart medical interventions, Dr. Fauci said.

“The virus has a playing field, as it were, to mutate,” Dr. Fauci said. “If you stop that and stop the replication, the viruses cannot mutate if they don’t replicate.”

A version of this article first appeared on Medscape.com.

New data on COVID-19 vaccines should serve as a “wake-up call” about the need to stop the spread of the SARS-CoV-2 virus among people and thus deprive it of opportunities to evolve its defenses, the top federal expert on infectious diseases said.

“The virus will continue to mutate and will mutate for its own selective advantage,” said Anthony S. Fauci, MD, director of the National Institute of Allergy and Infectious Diseases, at a Friday news conference organized by the White House.

The continued transmission of SARS-CoV-2 “gives the virus the chance to adapt to the forces, in this case the immune response, that’s trying to get rid of it,” Dr. Fauci said. “That’s where you get mutations.”

Federal health officials are working to boost the U.S. supply of COVID-19 vaccines, even as signals emerge about the extent that the virus is already evolving.

Data released this week about the Janssen/Johnson & Johnson (J&J) and Novavax COVID-19 vaccines in late-stage development provides further evidence that they may not protect as well against emerging variants, Dr. Fauci said.

“Mutations that lead to different lineage do have clinical consequences,” he said, while also emphasizing that the emerging vaccines appear to confer broad protection. Dr. Fauci earlier in the day addressed the “messaging challenge” for clinicians and researchers in discussing the results of the J&J vaccine trial, which appear to fall short of those reported for the two vaccines already approved and in use in the United States. He noted the benefits of possibly soon having more authorized vaccines to combat COVID-19. But continued community spread of the infection will foster conditions that can undermine the vaccines’ effectiveness.

“Even though the long-range effect in the sense of severe disease is still handled reasonably well by the vaccines, this is a wake-up call to all of us,” Dr. Fauci said.

Pharmaceutical scientists and executives and government health officials will need to work together to continue to develop vaccines that can outwit the emerging variants, he said.

On Jan. 29, J&J reported that its highly anticipated single-dose vaccine had shown its worst results in South Africa where many cases of COVID-19 were caused by infection with a SARS-CoV-2 variant from the B.1.351 lineage. The overall efficacy was 66% globally, 72% in the United States, and 57% in South Africa against moderate to severe SARS-CoV-2, J&J said.

Novavax on Jan. 28 reported an efficacy rate for its COVID-19 vaccine of 49.4% from a clinical trial conducted in South Africa, compared with an 89.3% rate from a U.K. study. There already have been attempts to estimate how well the Pfizer/BioNTech and Moderna vaccines can handle new variants of the virus. They both have been granted emergency-use authorization by the U.S. Food and Drug Administration.
 

‘Genomic surveillance’

The Centers for Disease Control and Prevention on Thursday reported the first U.S.-documented cases of the B.1.351 variant of SARS-CoV-2 in South Carolina. On Jan. 26, the first confirmed U.S. case of a highly transmissible Brazilian coronavirus variant was detected in Minnesota, state health officials said.

The CDC’s stepped-up “genomic surveillance” will help keep clinicians and researchers aware of how SARS-CoV-2 is changing, Dr. Fauci said.

Speaking at the same White House news conference, CDC director Rochelle Walensky, MD, MPH, said the two South Carolina cases of the B.1.351 variant were reported in different parts of the state and not believed to be epidemiologically linked. The people involved “did not have any travel history,” she added.

The SARS-CoV-2 mutations were expected to emerge at some point, as with any virus, but their appearance underscores the need for people to remain vigilant about precautions that can stop its spread, Dr. Walensky said.

She and Dr. Fauci both stressed the need for continued use of masks and social distancing and urged people to get COVID-19 vaccines as they become available. Continued community spread of the virus allows this global health threat to keep replicating, and thus increases its chances to thwart medical interventions, Dr. Fauci said.

“The virus has a playing field, as it were, to mutate,” Dr. Fauci said. “If you stop that and stop the replication, the viruses cannot mutate if they don’t replicate.”

A version of this article first appeared on Medscape.com.

An international team of researchers studying COVID-19 has made a startling and pivotal discovery: The virus appears to cause the body to make weapons to attack its own tissues.

The finding could unlock a number of COVID-19’s clinical mysteries. They include the puzzling collection of symptoms that can come with the infection; the persistence of symptoms in some people for months after they clear the virus, a phenomenon dubbed long COVID-19; and why some children and adults have a serious inflammatory syndrome, called multisystem inflammatory syndrome in children (MIS-C) or MIS in adults (MIS-A), after their infections.

“It suggests that the virus might be directly causing autoimmunity, which would be fascinating,” says lead study author Paul Utz, MD, who studies immunology and autoimmunity at Stanford (Calif.) University.

The study also deepens the question of whether other respiratory viruses might also break the body’s tolerance to itself, setting people up for autoimmune diseases like multiple sclerosis, rheumatoid arthritis, and lupus later in life.

Dr. Utz said he and his team are next going to study flu patients to see if that virus might also cause this phenomenon.

“My prediction is that it isn’t going to be specific just to SARS-CoV-2. I’m willing to bet that we will find this with other respiratory viruses,” he said.

The study comes on the heels of a handful of smaller, detailed investigations that have come to similar conclusions.

The study included data from more than 300 patients from four hospitals: two in California, one in Pennsylvania, and another in Germany.

Researchers used blood tests to study their immune responses as their infections progressed. Researchers looked for autoantibodies – weapons of the immune system that go rogue and launch an attack against the body’s own tissues. They compared these autoantibodies with those found in people who were not infected with the virus that causes COVID.

As previous studies have found, autoantibodies were more common after COVID – 50% of people hospitalized for their infections had autoantibodies, compared with less than 15% of those who were healthy and uninfected.

Some people with autoantibodies had little change in them as their infections progressed. That suggests the autoantibodies were there to begin with, possibly allowing the infection to burn out of control in the body.

“Their body is set up to get bad COVID, and it’s probably caused by the autoantibodies,” Dr. Utz said.

But in others, about 20% of people who had them, the autoantibodies became more common as the infection progressed, suggesting they were directly related to the viral infection, instead of being a preexisting condition.

Some of these were antibodies that attack key components of the immune system’s weapons against the virus, like interferon. Interferons are proteins that help infected cells call for reinforcements and can also interfere with a virus’s ability to copy itself. Taking them out is a powerful evasive tactic, and previous studies have shown that people who are born with genes that cause them to have lower interferon function, or who make autoantibodies against these proteins, appear to be at higher risk for life-threatening COVID infections.

“It seems to give the virus a powerful advantage,” said study author, John Wherry, PhD, who directs the Institute for Immunology at the University of Pennsylvania, Philadelphia. “Now your immune system, instead of having a tiny little hill to climb, is staring at Mount Everest. That really is devious.”

In addition to those that sabotage the immune system, some people in the study had autoantibodies against muscles and connective tissues that are seen in some rare disorders.

Dr. Utz said they started the study after seeing COVID patients with strange collections of symptoms that looked more like autoimmune diseases than viral infections – skin rashes, joint pain, fatigue, aching muscles, brain swelling, dry eyes, blood that clots easily, and inflamed blood vessels.

“One thing that’s very important to note is that we don’t know if these patients are going to go on to develop autoimmune disease,” Dr. Utz said. “I think we’ll be able to answer that question in the next 6-12 months as we follow the long haulers and study their samples.”

Dr. Utz said it will be important to study autoantibodies in long haulers to see if they can identify exactly which ones seem to be at work in the condition. If you can catch them early, it might be possible to treat those at risk for enduring symptoms with drugs that suppress the immune system.

What this means, he said, is that COVID will be with us for a long, long time.

“We have to realize that there’s going to be long-term damage from this virus for the survivors. Not just the long haulers, but all the people who have lung damage and heart damage and everything else. We’re going to be studying this virus and it’s badness for decades,” Dr. Utz said.

A version of this article first appeared on WebMD.com.

An international team of researchers studying COVID-19 has made a startling and pivotal discovery: The virus appears to cause the body to make weapons to attack its own tissues.

The finding could unlock a number of COVID-19’s clinical mysteries. They include the puzzling collection of symptoms that can come with the infection; the persistence of symptoms in some people for months after they clear the virus, a phenomenon dubbed long COVID-19; and why some children and adults have a serious inflammatory syndrome, called multisystem inflammatory syndrome in children (MIS-C) or MIS in adults (MIS-A), after their infections.

“It suggests that the virus might be directly causing autoimmunity, which would be fascinating,” says lead study author Paul Utz, MD, who studies immunology and autoimmunity at Stanford (Calif.) University.

The study also deepens the question of whether other respiratory viruses might also break the body’s tolerance to itself, setting people up for autoimmune diseases like multiple sclerosis, rheumatoid arthritis, and lupus later in life.

Dr. Utz said he and his team are next going to study flu patients to see if that virus might also cause this phenomenon.

“My prediction is that it isn’t going to be specific just to SARS-CoV-2. I’m willing to bet that we will find this with other respiratory viruses,” he said.

The study comes on the heels of a handful of smaller, detailed investigations that have come to similar conclusions.

The study included data from more than 300 patients from four hospitals: two in California, one in Pennsylvania, and another in Germany.

Researchers used blood tests to study their immune responses as their infections progressed. Researchers looked for autoantibodies – weapons of the immune system that go rogue and launch an attack against the body’s own tissues. They compared these autoantibodies with those found in people who were not infected with the virus that causes COVID.

As previous studies have found, autoantibodies were more common after COVID – 50% of people hospitalized for their infections had autoantibodies, compared with less than 15% of those who were healthy and uninfected.

Some people with autoantibodies had little change in them as their infections progressed. That suggests the autoantibodies were there to begin with, possibly allowing the infection to burn out of control in the body.

“Their body is set up to get bad COVID, and it’s probably caused by the autoantibodies,” Dr. Utz said.

But in others, about 20% of people who had them, the autoantibodies became more common as the infection progressed, suggesting they were directly related to the viral infection, instead of being a preexisting condition.

Some of these were antibodies that attack key components of the immune system’s weapons against the virus, like interferon. Interferons are proteins that help infected cells call for reinforcements and can also interfere with a virus’s ability to copy itself. Taking them out is a powerful evasive tactic, and previous studies have shown that people who are born with genes that cause them to have lower interferon function, or who make autoantibodies against these proteins, appear to be at higher risk for life-threatening COVID infections.

“It seems to give the virus a powerful advantage,” said study author, John Wherry, PhD, who directs the Institute for Immunology at the University of Pennsylvania, Philadelphia. “Now your immune system, instead of having a tiny little hill to climb, is staring at Mount Everest. That really is devious.”

In addition to those that sabotage the immune system, some people in the study had autoantibodies against muscles and connective tissues that are seen in some rare disorders.

Dr. Utz said they started the study after seeing COVID patients with strange collections of symptoms that looked more like autoimmune diseases than viral infections – skin rashes, joint pain, fatigue, aching muscles, brain swelling, dry eyes, blood that clots easily, and inflamed blood vessels.

“One thing that’s very important to note is that we don’t know if these patients are going to go on to develop autoimmune disease,” Dr. Utz said. “I think we’ll be able to answer that question in the next 6-12 months as we follow the long haulers and study their samples.”

Dr. Utz said it will be important to study autoantibodies in long haulers to see if they can identify exactly which ones seem to be at work in the condition. If you can catch them early, it might be possible to treat those at risk for enduring symptoms with drugs that suppress the immune system.

What this means, he said, is that COVID will be with us for a long, long time.

“We have to realize that there’s going to be long-term damage from this virus for the survivors. Not just the long haulers, but all the people who have lung damage and heart damage and everything else. We’re going to be studying this virus and it’s badness for decades,” Dr. Utz said.

A version of this article first appeared on WebMD.com.

An international team of researchers studying COVID-19 has made a startling and pivotal discovery: The virus appears to cause the body to make weapons to attack its own tissues.

The finding could unlock a number of COVID-19’s clinical mysteries. They include the puzzling collection of symptoms that can come with the infection; the persistence of symptoms in some people for months after they clear the virus, a phenomenon dubbed long COVID-19; and why some children and adults have a serious inflammatory syndrome, called multisystem inflammatory syndrome in children (MIS-C) or MIS in adults (MIS-A), after their infections.

“It suggests that the virus might be directly causing autoimmunity, which would be fascinating,” says lead study author Paul Utz, MD, who studies immunology and autoimmunity at Stanford (Calif.) University.

The study also deepens the question of whether other respiratory viruses might also break the body’s tolerance to itself, setting people up for autoimmune diseases like multiple sclerosis, rheumatoid arthritis, and lupus later in life.

Dr. Utz said he and his team are next going to study flu patients to see if that virus might also cause this phenomenon.

“My prediction is that it isn’t going to be specific just to SARS-CoV-2. I’m willing to bet that we will find this with other respiratory viruses,” he said.

The study comes on the heels of a handful of smaller, detailed investigations that have come to similar conclusions.

The study included data from more than 300 patients from four hospitals: two in California, one in Pennsylvania, and another in Germany.

Researchers used blood tests to study their immune responses as their infections progressed. Researchers looked for autoantibodies – weapons of the immune system that go rogue and launch an attack against the body’s own tissues. They compared these autoantibodies with those found in people who were not infected with the virus that causes COVID.

As previous studies have found, autoantibodies were more common after COVID – 50% of people hospitalized for their infections had autoantibodies, compared with less than 15% of those who were healthy and uninfected.

Some people with autoantibodies had little change in them as their infections progressed. That suggests the autoantibodies were there to begin with, possibly allowing the infection to burn out of control in the body.

“Their body is set up to get bad COVID, and it’s probably caused by the autoantibodies,” Dr. Utz said.

But in others, about 20% of people who had them, the autoantibodies became more common as the infection progressed, suggesting they were directly related to the viral infection, instead of being a preexisting condition.

Some of these were antibodies that attack key components of the immune system’s weapons against the virus, like interferon. Interferons are proteins that help infected cells call for reinforcements and can also interfere with a virus’s ability to copy itself. Taking them out is a powerful evasive tactic, and previous studies have shown that people who are born with genes that cause them to have lower interferon function, or who make autoantibodies against these proteins, appear to be at higher risk for life-threatening COVID infections.

“It seems to give the virus a powerful advantage,” said study author, John Wherry, PhD, who directs the Institute for Immunology at the University of Pennsylvania, Philadelphia. “Now your immune system, instead of having a tiny little hill to climb, is staring at Mount Everest. That really is devious.”

In addition to those that sabotage the immune system, some people in the study had autoantibodies against muscles and connective tissues that are seen in some rare disorders.

Dr. Utz said they started the study after seeing COVID patients with strange collections of symptoms that looked more like autoimmune diseases than viral infections – skin rashes, joint pain, fatigue, aching muscles, brain swelling, dry eyes, blood that clots easily, and inflamed blood vessels.

“One thing that’s very important to note is that we don’t know if these patients are going to go on to develop autoimmune disease,” Dr. Utz said. “I think we’ll be able to answer that question in the next 6-12 months as we follow the long haulers and study their samples.”

Dr. Utz said it will be important to study autoantibodies in long haulers to see if they can identify exactly which ones seem to be at work in the condition. If you can catch them early, it might be possible to treat those at risk for enduring symptoms with drugs that suppress the immune system.

What this means, he said, is that COVID will be with us for a long, long time.

“We have to realize that there’s going to be long-term damage from this virus for the survivors. Not just the long haulers, but all the people who have lung damage and heart damage and everything else. We’re going to be studying this virus and it’s badness for decades,” Dr. Utz said.

A version of this article first appeared on WebMD.com.

The COVID-19 variants that have emerged in the United Kingdom, Brazil, South Africa and now Southern California are eliciting two notably distinct responses from U.S. public health officials.

janiecbros/iStock/Getty Images Plus

First, broad concern. A variant that wreaked havoc in the United Kingdom, leading to a spike in cases and hospitalizations, is surfacing in a growing number of places in the United States. During the week of Jan. 24, another worrisome variant seen in Brazil surfaced in Minnesota. If these or other strains significantly change the way the virus transmits and attacks the body, as scientists fear they might, they could cause yet another prolonged surge in illness and death in the U.S., even as cases have begun to plateau and vaccines are rolling out.

On the other hand, variants aren’t novel or even uncommon in viral illnesses. The viruses that trigger common colds and flus regularly evolve. Even if a mutated strain of SARS-CoV-2, the virus that causes COVID-19, makes it more contagious or makes people sicker, the basic public health response stays the same: Monitor the virus, and any mutations, as it moves across communities. Use masking, testing, physical distancing, and quarantine to contain the spread.

The problem is that the U.S. has struggled with every step of its public health response in its first year of battle against COVID-19. And that raises the question of whether the nation will devote the attention and resources needed to outflank the virus as it evolves.

Researchers are quick to stress that a coronavirus mutation in itself is no cause for alarm. In the course of making millions and billions of copies as part of the infection process, small changes to a virus’s genome happen all the time as a function of evolutionary biology.

“The word ‘variant’ and the word ‘mutation’ have these scary connotations, and they aren’t necessarily scary,” said Kelly Wroblewski, director of infectious disease programs for the Association of Public Health Laboratories.

When a mutation rings public health alarms, it’s typically because it has combined with other mutations and, collectively, changed how the virus behaves. At that point, it may be named a variant. A variant can make a virus spread faster, or more easily jump between species. It can make a virus more successful at making people sicker, or change how our immune systems respond.

SARS-CoV-2 has been mutating for as long as we’ve known about it; mutations were identified by scientists throughout 2020. Though relevant scientifically – mutations can actually be helpful, acting like a fingerprint that allows scientists to track a virus’s spread – the identified strains mostly carried little concern for public health.

Then came the end of the year, when several variants began drawing scrutiny. One of the most concerning, first detected in the United Kingdom, appears to make the virus more transmissible. Emerging evidence suggests it also could be deadlier, though scientists are still debating that.

We know more about the U.K. variant than others not because it’s necessarily worse, but because the British have one of the best virus surveillance programs in the world, said William Hanage, PhD, an epidemiologist and a professor at Harvard University.

By contrast, the U.S. has one of the weakest genomic surveillance programs of any rich country, Dr. Hanage said. “As it is, people like me cobble together partnerships with places and try and beg them” for samples, he said on a recent call with reporters.

Other variant strains were identified in South Africa and Brazil, and they share some mutations with the U.K. variant. That those changes evolved independently in several parts of the world suggests they might present an evolutionary advantage for the virus. Yet another strain was recently identified in Southern California and flagged due to its increasing presence in hard-hit cities like Los Angeles.

The Southern California strain was detected because a team of researchers at Cedars-Sinai, a hospital and research center in Los Angeles, has unfettered access to patient samples. They were able to see that the strain made up a growing share of cases at the hospital in recent weeks, as well as among the limited number of other samples haphazardly collected at a network of labs in the region.

Not only does the U.S. do less genomic sequencing than most wealthy countries, but it also does its surveillance by happenstance. That means it takes longer to detect new strains and draw conclusions about them. It’s not yet clear, for example, whether that Southern California strain was truly worthy of a press release.

Vast swaths of America’s privatized and decentralized system of health care aren’t set up to send samples to public health or academic labs. “I’m more concerned about the systems to detect variants than I am these particular variants,” said Mark Pandori, PhD, director of Nevada’s public health laboratory and associate professor at the University of Nevada-Reno School of Medicine.

Limited genomic surveillance of viruses is yet another side effect of a fragmented and underfunded public health system that’s struggled to test, track contacts and get COVID-19 under control throughout the pandemic, Ms. Wroblewski said.

The nation’s public health infrastructure, generally funded on a disease-by-disease basis, has decent systems set up to sequence flu, foodborne illnesses and tuberculosis, but there has been no national strategy on COVID-19. “To look for variants, it needs to be a national picture if it’s going to be done well,” Ms. Wroblewski said.

The Biden administration has outlined a strategy for a national response to COVID-19, which includes expanded surveillance for variants.

So far, vaccines for COVID-19 appear to protect against the known variants. Moderna has said its vaccine is effective against the U.K. and South African strains, though it yields fewer antibodies in the face of the latter. The company is working to develop a revised dose of the vaccine that could be added to the current two-shot regimen as a precaution.

But a lot of damage can be done in the time it will take to roll out the current vaccine, let alone an update.

Even with limited sampling, the U.K. variant has been detected in more than two dozen U.S. states, and the Centers for Disease Control and Prevention has warned it could be the predominant strain in the U.S. by March. When it took off in the United Kingdom at the end of last year, it caused a swell in cases, overwhelmed hospitals, and led to a holiday lockdown. Whether the U.S. faces the same fate could depend on which strains it is competing against, and how the public behaves in the weeks ahead.

Already risky interactions among people could, on average, get a little riskier. Many researchers are calling for better masks and better indoor ventilation. But any updates on recommendations likely would play at the margins. Even if variants spread more easily, the same recommendations public health experts have been espousing for months – masking, physical distancing, and limiting time indoors with others – will be the best way to ward them off, said Kirsten Bibbins-Domingo, MD, a physician and professor at the University of California, San Francisco.

“It’s very unsexy what the solutions are,” Dr. Bibbins-Domingo said. “But we need everyone to do them.”

That doesn’t make the task simple. Masking remains controversial in many states, and the public’s patience for maintaining physical distance has worn thin.

Adding to the concerns: Though case numbers stabilized in many parts of the U.S. in January, they have stabilized at rates many times what they were during previous periods in the pandemic or in other parts of the world. Having all that virus in so many bodies creates more opportunities for new mutations and new variants to emerge.

“If we keep letting this thing sneak around, it’s going to get around all the measures we take against it, and that’s the worst possible thing,” said Nevada’s Dr. Pandori.

Compared with less virulent strains, a more contagious variant likely will require that more people be vaccinated before a community can see the benefits of widespread immunity. It’s a bleak outlook for a nation already falling behind in the race to vaccinate enough people to bring the pandemic under control.

“When your best solution is to ask people to do the things that they don’t like to do anyway, that’s very scary,” said Dr. Bibbins-Domingo.
 

This story was produced by KHN, which publishes California Healthline, an editorially independent service of the California Health Care Foundation.

The COVID-19 variants that have emerged in the United Kingdom, Brazil, South Africa and now Southern California are eliciting two notably distinct responses from U.S. public health officials.

janiecbros/iStock/Getty Images Plus

First, broad concern. A variant that wreaked havoc in the United Kingdom, leading to a spike in cases and hospitalizations, is surfacing in a growing number of places in the United States. During the week of Jan. 24, another worrisome variant seen in Brazil surfaced in Minnesota. If these or other strains significantly change the way the virus transmits and attacks the body, as scientists fear they might, they could cause yet another prolonged surge in illness and death in the U.S., even as cases have begun to plateau and vaccines are rolling out.

On the other hand, variants aren’t novel or even uncommon in viral illnesses. The viruses that trigger common colds and flus regularly evolve. Even if a mutated strain of SARS-CoV-2, the virus that causes COVID-19, makes it more contagious or makes people sicker, the basic public health response stays the same: Monitor the virus, and any mutations, as it moves across communities. Use masking, testing, physical distancing, and quarantine to contain the spread.

The problem is that the U.S. has struggled with every step of its public health response in its first year of battle against COVID-19. And that raises the question of whether the nation will devote the attention and resources needed to outflank the virus as it evolves.

Researchers are quick to stress that a coronavirus mutation in itself is no cause for alarm. In the course of making millions and billions of copies as part of the infection process, small changes to a virus’s genome happen all the time as a function of evolutionary biology.

“The word ‘variant’ and the word ‘mutation’ have these scary connotations, and they aren’t necessarily scary,” said Kelly Wroblewski, director of infectious disease programs for the Association of Public Health Laboratories.

When a mutation rings public health alarms, it’s typically because it has combined with other mutations and, collectively, changed how the virus behaves. At that point, it may be named a variant. A variant can make a virus spread faster, or more easily jump between species. It can make a virus more successful at making people sicker, or change how our immune systems respond.

SARS-CoV-2 has been mutating for as long as we’ve known about it; mutations were identified by scientists throughout 2020. Though relevant scientifically – mutations can actually be helpful, acting like a fingerprint that allows scientists to track a virus’s spread – the identified strains mostly carried little concern for public health.

Then came the end of the year, when several variants began drawing scrutiny. One of the most concerning, first detected in the United Kingdom, appears to make the virus more transmissible. Emerging evidence suggests it also could be deadlier, though scientists are still debating that.

We know more about the U.K. variant than others not because it’s necessarily worse, but because the British have one of the best virus surveillance programs in the world, said William Hanage, PhD, an epidemiologist and a professor at Harvard University.

By contrast, the U.S. has one of the weakest genomic surveillance programs of any rich country, Dr. Hanage said. “As it is, people like me cobble together partnerships with places and try and beg them” for samples, he said on a recent call with reporters.

Other variant strains were identified in South Africa and Brazil, and they share some mutations with the U.K. variant. That those changes evolved independently in several parts of the world suggests they might present an evolutionary advantage for the virus. Yet another strain was recently identified in Southern California and flagged due to its increasing presence in hard-hit cities like Los Angeles.

The Southern California strain was detected because a team of researchers at Cedars-Sinai, a hospital and research center in Los Angeles, has unfettered access to patient samples. They were able to see that the strain made up a growing share of cases at the hospital in recent weeks, as well as among the limited number of other samples haphazardly collected at a network of labs in the region.

Not only does the U.S. do less genomic sequencing than most wealthy countries, but it also does its surveillance by happenstance. That means it takes longer to detect new strains and draw conclusions about them. It’s not yet clear, for example, whether that Southern California strain was truly worthy of a press release.

Vast swaths of America’s privatized and decentralized system of health care aren’t set up to send samples to public health or academic labs. “I’m more concerned about the systems to detect variants than I am these particular variants,” said Mark Pandori, PhD, director of Nevada’s public health laboratory and associate professor at the University of Nevada-Reno School of Medicine.

Limited genomic surveillance of viruses is yet another side effect of a fragmented and underfunded public health system that’s struggled to test, track contacts and get COVID-19 under control throughout the pandemic, Ms. Wroblewski said.

The nation’s public health infrastructure, generally funded on a disease-by-disease basis, has decent systems set up to sequence flu, foodborne illnesses and tuberculosis, but there has been no national strategy on COVID-19. “To look for variants, it needs to be a national picture if it’s going to be done well,” Ms. Wroblewski said.

The Biden administration has outlined a strategy for a national response to COVID-19, which includes expanded surveillance for variants.

So far, vaccines for COVID-19 appear to protect against the known variants. Moderna has said its vaccine is effective against the U.K. and South African strains, though it yields fewer antibodies in the face of the latter. The company is working to develop a revised dose of the vaccine that could be added to the current two-shot regimen as a precaution.

But a lot of damage can be done in the time it will take to roll out the current vaccine, let alone an update.

Even with limited sampling, the U.K. variant has been detected in more than two dozen U.S. states, and the Centers for Disease Control and Prevention has warned it could be the predominant strain in the U.S. by March. When it took off in the United Kingdom at the end of last year, it caused a swell in cases, overwhelmed hospitals, and led to a holiday lockdown. Whether the U.S. faces the same fate could depend on which strains it is competing against, and how the public behaves in the weeks ahead.

Already risky interactions among people could, on average, get a little riskier. Many researchers are calling for better masks and better indoor ventilation. But any updates on recommendations likely would play at the margins. Even if variants spread more easily, the same recommendations public health experts have been espousing for months – masking, physical distancing, and limiting time indoors with others – will be the best way to ward them off, said Kirsten Bibbins-Domingo, MD, a physician and professor at the University of California, San Francisco.

“It’s very unsexy what the solutions are,” Dr. Bibbins-Domingo said. “But we need everyone to do them.”

That doesn’t make the task simple. Masking remains controversial in many states, and the public’s patience for maintaining physical distance has worn thin.

Adding to the concerns: Though case numbers stabilized in many parts of the U.S. in January, they have stabilized at rates many times what they were during previous periods in the pandemic or in other parts of the world. Having all that virus in so many bodies creates more opportunities for new mutations and new variants to emerge.

“If we keep letting this thing sneak around, it’s going to get around all the measures we take against it, and that’s the worst possible thing,” said Nevada’s Dr. Pandori.

Compared with less virulent strains, a more contagious variant likely will require that more people be vaccinated before a community can see the benefits of widespread immunity. It’s a bleak outlook for a nation already falling behind in the race to vaccinate enough people to bring the pandemic under control.

“When your best solution is to ask people to do the things that they don’t like to do anyway, that’s very scary,” said Dr. Bibbins-Domingo.
 

This story was produced by KHN, which publishes California Healthline, an editorially independent service of the California Health Care Foundation.

The COVID-19 variants that have emerged in the United Kingdom, Brazil, South Africa and now Southern California are eliciting two notably distinct responses from U.S. public health officials.

janiecbros/iStock/Getty Images Plus

First, broad concern. A variant that wreaked havoc in the United Kingdom, leading to a spike in cases and hospitalizations, is surfacing in a growing number of places in the United States. During the week of Jan. 24, another worrisome variant seen in Brazil surfaced in Minnesota. If these or other strains significantly change the way the virus transmits and attacks the body, as scientists fear they might, they could cause yet another prolonged surge in illness and death in the U.S., even as cases have begun to plateau and vaccines are rolling out.

On the other hand, variants aren’t novel or even uncommon in viral illnesses. The viruses that trigger common colds and flus regularly evolve. Even if a mutated strain of SARS-CoV-2, the virus that causes COVID-19, makes it more contagious or makes people sicker, the basic public health response stays the same: Monitor the virus, and any mutations, as it moves across communities. Use masking, testing, physical distancing, and quarantine to contain the spread.

The problem is that the U.S. has struggled with every step of its public health response in its first year of battle against COVID-19. And that raises the question of whether the nation will devote the attention and resources needed to outflank the virus as it evolves.

Researchers are quick to stress that a coronavirus mutation in itself is no cause for alarm. In the course of making millions and billions of copies as part of the infection process, small changes to a virus’s genome happen all the time as a function of evolutionary biology.

“The word ‘variant’ and the word ‘mutation’ have these scary connotations, and they aren’t necessarily scary,” said Kelly Wroblewski, director of infectious disease programs for the Association of Public Health Laboratories.

When a mutation rings public health alarms, it’s typically because it has combined with other mutations and, collectively, changed how the virus behaves. At that point, it may be named a variant. A variant can make a virus spread faster, or more easily jump between species. It can make a virus more successful at making people sicker, or change how our immune systems respond.

SARS-CoV-2 has been mutating for as long as we’ve known about it; mutations were identified by scientists throughout 2020. Though relevant scientifically – mutations can actually be helpful, acting like a fingerprint that allows scientists to track a virus’s spread – the identified strains mostly carried little concern for public health.

Then came the end of the year, when several variants began drawing scrutiny. One of the most concerning, first detected in the United Kingdom, appears to make the virus more transmissible. Emerging evidence suggests it also could be deadlier, though scientists are still debating that.

We know more about the U.K. variant than others not because it’s necessarily worse, but because the British have one of the best virus surveillance programs in the world, said William Hanage, PhD, an epidemiologist and a professor at Harvard University.

By contrast, the U.S. has one of the weakest genomic surveillance programs of any rich country, Dr. Hanage said. “As it is, people like me cobble together partnerships with places and try and beg them” for samples, he said on a recent call with reporters.

Other variant strains were identified in South Africa and Brazil, and they share some mutations with the U.K. variant. That those changes evolved independently in several parts of the world suggests they might present an evolutionary advantage for the virus. Yet another strain was recently identified in Southern California and flagged due to its increasing presence in hard-hit cities like Los Angeles.

The Southern California strain was detected because a team of researchers at Cedars-Sinai, a hospital and research center in Los Angeles, has unfettered access to patient samples. They were able to see that the strain made up a growing share of cases at the hospital in recent weeks, as well as among the limited number of other samples haphazardly collected at a network of labs in the region.

Not only does the U.S. do less genomic sequencing than most wealthy countries, but it also does its surveillance by happenstance. That means it takes longer to detect new strains and draw conclusions about them. It’s not yet clear, for example, whether that Southern California strain was truly worthy of a press release.

Vast swaths of America’s privatized and decentralized system of health care aren’t set up to send samples to public health or academic labs. “I’m more concerned about the systems to detect variants than I am these particular variants,” said Mark Pandori, PhD, director of Nevada’s public health laboratory and associate professor at the University of Nevada-Reno School of Medicine.

Limited genomic surveillance of viruses is yet another side effect of a fragmented and underfunded public health system that’s struggled to test, track contacts and get COVID-19 under control throughout the pandemic, Ms. Wroblewski said.

The nation’s public health infrastructure, generally funded on a disease-by-disease basis, has decent systems set up to sequence flu, foodborne illnesses and tuberculosis, but there has been no national strategy on COVID-19. “To look for variants, it needs to be a national picture if it’s going to be done well,” Ms. Wroblewski said.

The Biden administration has outlined a strategy for a national response to COVID-19, which includes expanded surveillance for variants.

So far, vaccines for COVID-19 appear to protect against the known variants. Moderna has said its vaccine is effective against the U.K. and South African strains, though it yields fewer antibodies in the face of the latter. The company is working to develop a revised dose of the vaccine that could be added to the current two-shot regimen as a precaution.

But a lot of damage can be done in the time it will take to roll out the current vaccine, let alone an update.

Even with limited sampling, the U.K. variant has been detected in more than two dozen U.S. states, and the Centers for Disease Control and Prevention has warned it could be the predominant strain in the U.S. by March. When it took off in the United Kingdom at the end of last year, it caused a swell in cases, overwhelmed hospitals, and led to a holiday lockdown. Whether the U.S. faces the same fate could depend on which strains it is competing against, and how the public behaves in the weeks ahead.

Already risky interactions among people could, on average, get a little riskier. Many researchers are calling for better masks and better indoor ventilation. But any updates on recommendations likely would play at the margins. Even if variants spread more easily, the same recommendations public health experts have been espousing for months – masking, physical distancing, and limiting time indoors with others – will be the best way to ward them off, said Kirsten Bibbins-Domingo, MD, a physician and professor at the University of California, San Francisco.

“It’s very unsexy what the solutions are,” Dr. Bibbins-Domingo said. “But we need everyone to do them.”

That doesn’t make the task simple. Masking remains controversial in many states, and the public’s patience for maintaining physical distance has worn thin.

Adding to the concerns: Though case numbers stabilized in many parts of the U.S. in January, they have stabilized at rates many times what they were during previous periods in the pandemic or in other parts of the world. Having all that virus in so many bodies creates more opportunities for new mutations and new variants to emerge.

“If we keep letting this thing sneak around, it’s going to get around all the measures we take against it, and that’s the worst possible thing,” said Nevada’s Dr. Pandori.

Compared with less virulent strains, a more contagious variant likely will require that more people be vaccinated before a community can see the benefits of widespread immunity. It’s a bleak outlook for a nation already falling behind in the race to vaccinate enough people to bring the pandemic under control.

“When your best solution is to ask people to do the things that they don’t like to do anyway, that’s very scary,” said Dr. Bibbins-Domingo.
 

This story was produced by KHN, which publishes California Healthline, an editorially independent service of the California Health Care Foundation.

Experts discuss how to best protect people with diabetes from serious COVID-19 outcomes in a newly published article that summarizes in-depth discussions on the topic from a conference held online last year.

Lead author and Diabetes Technology Society founder and director David C. Klonoff, MD, said in an interview: “To my knowledge this is the largest article or learning that has been written anywhere ever about the co-occurrence of COVID-19 and diabetes and how COVID-19 affects diabetes ... There are a lot of different dimensions.” 

The 37-page report covers all sessions from the Virtual International COVID-19 and Diabetes Summit, held Aug. 26-27, 2020, which had 800 attendees from six continents, on topics including pathophysiology and COVID-19 risk factors, the impact of social determinants of health on diabetes and COVID-19, and psychological aspects of the COVID-19 pandemic for people with diabetes.

The freely available report was published online Jan. 21 in the Journal of Diabetes Science and Technology by Jennifer Y. Zhang of the Diabetes Technology Society, Burlingame, Calif., and colleagues.

Other topics include medications and vaccines, outpatient diabetes management during the COVID-19 pandemic and the growth of telehealth, inpatient management of diabetes in patients with or without COVID-19, ethical considerations, children, pregnancy, economics of care for COVID-19, government policy, regulation of tests and treatments, patient surveillance/privacy, and research gaps and opportunities.

“A comprehensive report like this is so important because it covers such a wide range of topics that are all relevant when it comes to protecting patients with diabetes during a pandemic. Our report aims to bring together all these different aspects of policy during the pandemic, patient physiology, and patient psychology, so I hope it will be widely read and widely appreciated,” Ms. Zhang said in an interview.

Two important clinical trends arising as a result of the pandemic – the advent of telehealth in diabetes management and the use of continuous glucose monitoring (CGM) in hospital – are expected to continue even after COVID-19 abates, said Dr. Klonoff, medical director of the Diabetes Research Institute at Mills-Peninsula Medical Center, San Mateo, Calif.


 

Telehealth in diabetes here to stay, in U.S. at least  

Dr. Klonoff noted that with diabetes telehealth, or “telediabetes” as it’s been dubbed, by using downloaded device data patients don’t have to travel, pay for parking, or take as much time off work. “There are advantages ... patients really like it,” he said.

And for health care providers, an advantage of remote visits is that the clinician can look at the patient while reviewing the patient’s data. “With telehealth for diabetes, the patient’s face and the software data are right next to each other on the same screen. Even as I’m typing I’m looking at the patient ... I consider that a huge advantage,” Dr. Klonoff said.

Rule changes early in the pandemic made the shift to telehealth in the United States possible, he said.

“Fortunately, Medicare and other payers are covering telehealth. It used to be there was no coverage, so that was a damper. Now that it’s covered I don’t think that’s going to go back. Everybody likes it,” he said. 
 

CGM in hospitals helps detect hypoglycemia on wards

Regarding the increase of inpatient CGM (continuous glucose monitoring) prompted by the need to minimize patient exposure of nursing staff during the pandemic and the relaxing of Food and Drug Administration rules about its use, Dr. Klonoff said this phenomenon has led to two other positive developments.

“For FDA, it’s actually an opportunity to see some data collected. To do a clinical trial [prior to] March 2020 you had to go through a lot of processes to do a study. Once it becomes part of clinical care, then you can collect a lot of data,” he noted.   

Moreover, Dr. Klonoff said there’s an important new area where hospital use of CGM is emerging: detection of hypoglycemia on wards.

“When a patient is in the ICU, if they become hypoglycemic or hyperglycemic it will likely be detected. But on the wards, they simply don’t get the same attention. Just about every doctor has had a case where somebody drifted into hypoglycemia that wasn’t recognized and maybe even died,” he explained.

If, however, “patients treated with insulin could all have CGMs that would be so useful. It would send out an alarm. A lot of times people don’t eat when you think they will. Suddenly the insulin dose is inappropriate and the nurse didn’t realize. Or, if IV nutrition stops and the insulin is given [it can be harmful].”

Another example, he said, is a common scenario when insulin is used in patients who are treated with steroids. “They need insulin, but then the steroid is decreased and the insulin dose isn’t decreased fast enough. All those situations can be helped with CGM.”

Overall, he concluded, COVID-19 has provided many lessons, which are “expanding our horizons.”

Ms. Zhang has reported no relevant financial relationships. Dr. Klonoff has reported being a consultant for Dexcom, EOFlow, Fractyl, Lifecare, Novo Nordisk, Roche Diagnostics, Samsung, and Thirdwayv.

A version of this article first appeared on Medscape.com.

Experts discuss how to best protect people with diabetes from serious COVID-19 outcomes in a newly published article that summarizes in-depth discussions on the topic from a conference held online last year.

Lead author and Diabetes Technology Society founder and director David C. Klonoff, MD, said in an interview: “To my knowledge this is the largest article or learning that has been written anywhere ever about the co-occurrence of COVID-19 and diabetes and how COVID-19 affects diabetes ... There are a lot of different dimensions.” 

The 37-page report covers all sessions from the Virtual International COVID-19 and Diabetes Summit, held Aug. 26-27, 2020, which had 800 attendees from six continents, on topics including pathophysiology and COVID-19 risk factors, the impact of social determinants of health on diabetes and COVID-19, and psychological aspects of the COVID-19 pandemic for people with diabetes.

The freely available report was published online Jan. 21 in the Journal of Diabetes Science and Technology by Jennifer Y. Zhang of the Diabetes Technology Society, Burlingame, Calif., and colleagues.

Other topics include medications and vaccines, outpatient diabetes management during the COVID-19 pandemic and the growth of telehealth, inpatient management of diabetes in patients with or without COVID-19, ethical considerations, children, pregnancy, economics of care for COVID-19, government policy, regulation of tests and treatments, patient surveillance/privacy, and research gaps and opportunities.

“A comprehensive report like this is so important because it covers such a wide range of topics that are all relevant when it comes to protecting patients with diabetes during a pandemic. Our report aims to bring together all these different aspects of policy during the pandemic, patient physiology, and patient psychology, so I hope it will be widely read and widely appreciated,” Ms. Zhang said in an interview.

Two important clinical trends arising as a result of the pandemic – the advent of telehealth in diabetes management and the use of continuous glucose monitoring (CGM) in hospital – are expected to continue even after COVID-19 abates, said Dr. Klonoff, medical director of the Diabetes Research Institute at Mills-Peninsula Medical Center, San Mateo, Calif.


 

Telehealth in diabetes here to stay, in U.S. at least  

Dr. Klonoff noted that with diabetes telehealth, or “telediabetes” as it’s been dubbed, by using downloaded device data patients don’t have to travel, pay for parking, or take as much time off work. “There are advantages ... patients really like it,” he said.

And for health care providers, an advantage of remote visits is that the clinician can look at the patient while reviewing the patient’s data. “With telehealth for diabetes, the patient’s face and the software data are right next to each other on the same screen. Even as I’m typing I’m looking at the patient ... I consider that a huge advantage,” Dr. Klonoff said.

Rule changes early in the pandemic made the shift to telehealth in the United States possible, he said.

“Fortunately, Medicare and other payers are covering telehealth. It used to be there was no coverage, so that was a damper. Now that it’s covered I don’t think that’s going to go back. Everybody likes it,” he said. 
 

CGM in hospitals helps detect hypoglycemia on wards

Regarding the increase of inpatient CGM (continuous glucose monitoring) prompted by the need to minimize patient exposure of nursing staff during the pandemic and the relaxing of Food and Drug Administration rules about its use, Dr. Klonoff said this phenomenon has led to two other positive developments.

“For FDA, it’s actually an opportunity to see some data collected. To do a clinical trial [prior to] March 2020 you had to go through a lot of processes to do a study. Once it becomes part of clinical care, then you can collect a lot of data,” he noted.   

Moreover, Dr. Klonoff said there’s an important new area where hospital use of CGM is emerging: detection of hypoglycemia on wards.

“When a patient is in the ICU, if they become hypoglycemic or hyperglycemic it will likely be detected. But on the wards, they simply don’t get the same attention. Just about every doctor has had a case where somebody drifted into hypoglycemia that wasn’t recognized and maybe even died,” he explained.

If, however, “patients treated with insulin could all have CGMs that would be so useful. It would send out an alarm. A lot of times people don’t eat when you think they will. Suddenly the insulin dose is inappropriate and the nurse didn’t realize. Or, if IV nutrition stops and the insulin is given [it can be harmful].”

Another example, he said, is a common scenario when insulin is used in patients who are treated with steroids. “They need insulin, but then the steroid is decreased and the insulin dose isn’t decreased fast enough. All those situations can be helped with CGM.”

Overall, he concluded, COVID-19 has provided many lessons, which are “expanding our horizons.”

Ms. Zhang has reported no relevant financial relationships. Dr. Klonoff has reported being a consultant for Dexcom, EOFlow, Fractyl, Lifecare, Novo Nordisk, Roche Diagnostics, Samsung, and Thirdwayv.

A version of this article first appeared on Medscape.com.

Experts discuss how to best protect people with diabetes from serious COVID-19 outcomes in a newly published article that summarizes in-depth discussions on the topic from a conference held online last year.

Lead author and Diabetes Technology Society founder and director David C. Klonoff, MD, said in an interview: “To my knowledge this is the largest article or learning that has been written anywhere ever about the co-occurrence of COVID-19 and diabetes and how COVID-19 affects diabetes ... There are a lot of different dimensions.” 

The 37-page report covers all sessions from the Virtual International COVID-19 and Diabetes Summit, held Aug. 26-27, 2020, which had 800 attendees from six continents, on topics including pathophysiology and COVID-19 risk factors, the impact of social determinants of health on diabetes and COVID-19, and psychological aspects of the COVID-19 pandemic for people with diabetes.

The freely available report was published online Jan. 21 in the Journal of Diabetes Science and Technology by Jennifer Y. Zhang of the Diabetes Technology Society, Burlingame, Calif., and colleagues.

Other topics include medications and vaccines, outpatient diabetes management during the COVID-19 pandemic and the growth of telehealth, inpatient management of diabetes in patients with or without COVID-19, ethical considerations, children, pregnancy, economics of care for COVID-19, government policy, regulation of tests and treatments, patient surveillance/privacy, and research gaps and opportunities.

“A comprehensive report like this is so important because it covers such a wide range of topics that are all relevant when it comes to protecting patients with diabetes during a pandemic. Our report aims to bring together all these different aspects of policy during the pandemic, patient physiology, and patient psychology, so I hope it will be widely read and widely appreciated,” Ms. Zhang said in an interview.

Two important clinical trends arising as a result of the pandemic – the advent of telehealth in diabetes management and the use of continuous glucose monitoring (CGM) in hospital – are expected to continue even after COVID-19 abates, said Dr. Klonoff, medical director of the Diabetes Research Institute at Mills-Peninsula Medical Center, San Mateo, Calif.


 

Telehealth in diabetes here to stay, in U.S. at least  

Dr. Klonoff noted that with diabetes telehealth, or “telediabetes” as it’s been dubbed, by using downloaded device data patients don’t have to travel, pay for parking, or take as much time off work. “There are advantages ... patients really like it,” he said.

And for health care providers, an advantage of remote visits is that the clinician can look at the patient while reviewing the patient’s data. “With telehealth for diabetes, the patient’s face and the software data are right next to each other on the same screen. Even as I’m typing I’m looking at the patient ... I consider that a huge advantage,” Dr. Klonoff said.

Rule changes early in the pandemic made the shift to telehealth in the United States possible, he said.

“Fortunately, Medicare and other payers are covering telehealth. It used to be there was no coverage, so that was a damper. Now that it’s covered I don’t think that’s going to go back. Everybody likes it,” he said. 
 

CGM in hospitals helps detect hypoglycemia on wards

Regarding the increase of inpatient CGM (continuous glucose monitoring) prompted by the need to minimize patient exposure of nursing staff during the pandemic and the relaxing of Food and Drug Administration rules about its use, Dr. Klonoff said this phenomenon has led to two other positive developments.

“For FDA, it’s actually an opportunity to see some data collected. To do a clinical trial [prior to] March 2020 you had to go through a lot of processes to do a study. Once it becomes part of clinical care, then you can collect a lot of data,” he noted.   

Moreover, Dr. Klonoff said there’s an important new area where hospital use of CGM is emerging: detection of hypoglycemia on wards.

“When a patient is in the ICU, if they become hypoglycemic or hyperglycemic it will likely be detected. But on the wards, they simply don’t get the same attention. Just about every doctor has had a case where somebody drifted into hypoglycemia that wasn’t recognized and maybe even died,” he explained.

If, however, “patients treated with insulin could all have CGMs that would be so useful. It would send out an alarm. A lot of times people don’t eat when you think they will. Suddenly the insulin dose is inappropriate and the nurse didn’t realize. Or, if IV nutrition stops and the insulin is given [it can be harmful].”

Another example, he said, is a common scenario when insulin is used in patients who are treated with steroids. “They need insulin, but then the steroid is decreased and the insulin dose isn’t decreased fast enough. All those situations can be helped with CGM.”

Overall, he concluded, COVID-19 has provided many lessons, which are “expanding our horizons.”

Ms. Zhang has reported no relevant financial relationships. Dr. Klonoff has reported being a consultant for Dexcom, EOFlow, Fractyl, Lifecare, Novo Nordisk, Roche Diagnostics, Samsung, and Thirdwayv.

A version of this article first appeared on Medscape.com.