Infectious Disease Practitioner

The Trump administration can move forward with expanding a rule that makes it more difficult for immigrants to remain in the United States if they receive health care assistance, the U.S. Supreme Court ruled in a 5-4 vote.

Courtesy Fred Schilling, Collection of the Supreme Court of the United States

The Feb. 21 order allows the administration to broaden the so-called “public charge rule” while legal challenges against the expanded regulation continue in the lower courts. The Supreme Court’s decision, which lifts a preliminary injunction against the expansion, applies to enforcement only in Illinois, where a district court blocked the revised rule from moving forward in October 2019. The Supreme Court’s measure follows another 5-4 order in January, in which justices lifted a nationwide injunction against the revised rule.

Under the long-standing public charge rule, immigration officials can refuse to admit immigrants into the United States or can deny them permanent legal status if they are deemed likely to become a public charge. Previously, immigration officers considered cash aid, such as Temporary Assistance for Needy Families or long-term institutionalized care, as potential public charge reasons for denial.

The revised regulation allows officials to consider previously excluded programs in their determination, including nonemergency Medicaid, the Supplemental Nutrition Assistance Program, and several housing programs. Use of these programs for more than 12 months in the aggregate during a 36-month period may result in a “public charge” designation and lead to green card denial.

Eight legal challenges were immediately filed against the rule changes, including a complaint issued by 14 states. At least five trial courts have since blocked the measure, while appeals courts have lifted some of the injunctions and upheld enforcement.

In its Jan. 27 order lifting the nationwide injunction, Associate Justice Neil M. Gorsuch wrote that nationwide injunctions are being overused by trial courts with negative consequences.

“The real problem here is the increasingly common practice of trial courts ordering relief that transcends the cases before them. Whether framed as injunctions of ‘nationwide,’ ‘universal,’ or ‘cosmic’ scope, these orders share the same basic flaw – they direct how the defendant must act toward persons who are not parties to the case,” he wrote. “It has become increasingly apparent that this court must, at some point, confront these important objections to this increasingly widespread practice. As the brief and furious history of the regulation before us illustrates, the routine issuance of universal injunctions is patently unworkable, sowing chaos for litigants, the government, courts, and all those affected by these conflicting decisions.”

In the court’s Feb. 21 order lifting the injunction in Illinois, justices gave no explanation for overturning the lower court’s injunction. However, Associate Justice Sonia Sotomayor issued a sharply-worded dissent, criticizing her fellow justices for allowing the rule to proceed.

“In sum, the government’s only claimed hardship is that it must enforce an existing interpretation of an immigration rule in one state – just as it has done for the past 20 years – while an updated version of the rule takes effect in the remaining 49,” she wrote. “The government has not quantified or explained any burdens that would arise from this state of the world.”

ACA cases still in limbo

Meanwhile, the Supreme Court still has not decided whether it will hear Texas v. United States, a case that could effectively dismantle the Affordable Care Act.

The high court was expected to announce whether it would take the high-profile case at a private Feb. 21 conference, but the justices have released no update. The case was relisted for consideration at the court’s Feb. 28 conference.

Texas v. United States stems from a lawsuit by 20 Republican state attorneys general and governors that was filed after Congress zeroed out the ACA’s individual mandate penalty in 2017. The plaintiffs contend the now-valueless mandate is no longer constitutional and thus, the entire ACA should be struck down. Because the Trump administration declined to defend the law, a coalition of Democratic attorneys general and governors intervened in the case as defendants.

In 2018, a Texas district court ruled in favor of the plaintiffs and declared the entire health care law invalid. The 5th U.S. Circuit Court of Appeals partially affirmed the district court’s decision, ruling that the mandate was unconstitutional, but sending the case back to the lower court for more analysis on severability. The Democratic attorneys general and governors appealed the decision to the U.S. Supreme Court.

If the Supreme Court agrees to hear the challenge, the court could fast-track the case and schedule arguments for the current term or wait until its next term, which starts in October 2020. If justices decline to hear the case, the challenge will remain with the district court for more analysis about the law’s severability.

Another ACA-related case – Maine Community Health Options v. U.S. – also remains in limbo. Justices heard the case, which was consolidated with two similar challenges, on Dec. 10, 2019, but still have not issued a decision.

The consolidated challenges center on whether the federal government owes insurers billions based on an Affordable Care Act provision intended to help health plans mitigate risk under the law. The ACA’s risk corridor program required the U.S. Department of Health & Human Services to collect funds from profitable insurers that offered qualified health plans under the exchanges and distribute the funds to insurers with excessive losses. Collections from profitable insurers under the program fell short in 2014, 2015, and 2016, while losses steadily grew, resulting in the HHS paying about 12 cents on the dollar in payments to insurers. More than 150 insurers now allege they were shortchanged and they want the Supreme Court to force the government to reimburse them to the tune of $12 billion.

The Department of Justice counters that the government is not required to pay the insurers because of appropriations measures passed by Congress in 2014 and in later years that limited the funding available to compensate insurers for their losses.

The federal government and insurers have each experienced wins and losses at the lower court level. Most recently, the U.S. Court of Appeals for the Federal Circuit decided in favor of the government, ruling that while the ACA required the government to compensate the insurers for their losses, the appropriations measures repealed or suspended that requirement.

A Supreme Court decision in the case could come as soon as Feb. 26.

Court to hear women’s health cases

Two closely watched reproductive health cases will go before the court this spring.

On March 4, justices will hear oral arguments in June Medical Services v. Russo, regarding the constitutionality of a Louisiana law that requires physicians performing abortions to have admitting privileges at a nearby hospital. Doctors who perform abortions without admitting privileges at a hospital within 30 miles face fines and imprisonment, according to the state law, originally passed in 2014. Clinics that employ such doctors can also have their licenses revoked.

June Medical Services LLC, a women’s health clinic, sued over the law. A district court ruled in favor of the plaintiff, but the 5th U.S. Circuit Court of Appeals reversed and upheld Louisiana’s law. The clinic appealed to the U.S. Supreme Court. Louisiana officials argue the challenge should be dismissed, and the law allowed to proceed, because the plaintiffs lack standing.

The Supreme Court in 2016 heard a similar case – Whole Woman’s Health v. Hellerstedt – concerning a comparable law in Texas. In that case, justices struck down the measure as unconstitutional.

And on April 29, justices will hear arguments in Little Sisters of the Poor v. Pennsylvania, a consolidated case about whether the Trump administration acted properly when it expanded exemptions under the Affordable Care Act’s contraceptive mandate. Entities that object to providing contraception on the basis of religious beliefs can opt out of complying with the mandate, according to the 2018 regulations. Additionally, nonprofit organizations and small businesses that have nonreligious moral convictions against the mandate can skip compliance. A number of states and entities sued over the new rules.

A federal appeals court temporarily barred the regulations from moving forward, ruling the plaintiffs were likely to succeed in proving the Trump administration did not follow appropriate procedures when it promulgated the new rules and that the regulations were not authorized under the ACA.

Justices will decide whether the parties have standing in the case, whether the Trump administration followed correct rule-making procedures, and if the regulations can stand.

[email protected]

The Trump administration can move forward with expanding a rule that makes it more difficult for immigrants to remain in the United States if they receive health care assistance, the U.S. Supreme Court ruled in a 5-4 vote.

Courtesy Fred Schilling, Collection of the Supreme Court of the United States

The Feb. 21 order allows the administration to broaden the so-called “public charge rule” while legal challenges against the expanded regulation continue in the lower courts. The Supreme Court’s decision, which lifts a preliminary injunction against the expansion, applies to enforcement only in Illinois, where a district court blocked the revised rule from moving forward in October 2019. The Supreme Court’s measure follows another 5-4 order in January, in which justices lifted a nationwide injunction against the revised rule.

Under the long-standing public charge rule, immigration officials can refuse to admit immigrants into the United States or can deny them permanent legal status if they are deemed likely to become a public charge. Previously, immigration officers considered cash aid, such as Temporary Assistance for Needy Families or long-term institutionalized care, as potential public charge reasons for denial.

The revised regulation allows officials to consider previously excluded programs in their determination, including nonemergency Medicaid, the Supplemental Nutrition Assistance Program, and several housing programs. Use of these programs for more than 12 months in the aggregate during a 36-month period may result in a “public charge” designation and lead to green card denial.

Eight legal challenges were immediately filed against the rule changes, including a complaint issued by 14 states. At least five trial courts have since blocked the measure, while appeals courts have lifted some of the injunctions and upheld enforcement.

In its Jan. 27 order lifting the nationwide injunction, Associate Justice Neil M. Gorsuch wrote that nationwide injunctions are being overused by trial courts with negative consequences.

“The real problem here is the increasingly common practice of trial courts ordering relief that transcends the cases before them. Whether framed as injunctions of ‘nationwide,’ ‘universal,’ or ‘cosmic’ scope, these orders share the same basic flaw – they direct how the defendant must act toward persons who are not parties to the case,” he wrote. “It has become increasingly apparent that this court must, at some point, confront these important objections to this increasingly widespread practice. As the brief and furious history of the regulation before us illustrates, the routine issuance of universal injunctions is patently unworkable, sowing chaos for litigants, the government, courts, and all those affected by these conflicting decisions.”

In the court’s Feb. 21 order lifting the injunction in Illinois, justices gave no explanation for overturning the lower court’s injunction. However, Associate Justice Sonia Sotomayor issued a sharply-worded dissent, criticizing her fellow justices for allowing the rule to proceed.

“In sum, the government’s only claimed hardship is that it must enforce an existing interpretation of an immigration rule in one state – just as it has done for the past 20 years – while an updated version of the rule takes effect in the remaining 49,” she wrote. “The government has not quantified or explained any burdens that would arise from this state of the world.”

ACA cases still in limbo

Meanwhile, the Supreme Court still has not decided whether it will hear Texas v. United States, a case that could effectively dismantle the Affordable Care Act.

The high court was expected to announce whether it would take the high-profile case at a private Feb. 21 conference, but the justices have released no update. The case was relisted for consideration at the court’s Feb. 28 conference.

Texas v. United States stems from a lawsuit by 20 Republican state attorneys general and governors that was filed after Congress zeroed out the ACA’s individual mandate penalty in 2017. The plaintiffs contend the now-valueless mandate is no longer constitutional and thus, the entire ACA should be struck down. Because the Trump administration declined to defend the law, a coalition of Democratic attorneys general and governors intervened in the case as defendants.

In 2018, a Texas district court ruled in favor of the plaintiffs and declared the entire health care law invalid. The 5th U.S. Circuit Court of Appeals partially affirmed the district court’s decision, ruling that the mandate was unconstitutional, but sending the case back to the lower court for more analysis on severability. The Democratic attorneys general and governors appealed the decision to the U.S. Supreme Court.

If the Supreme Court agrees to hear the challenge, the court could fast-track the case and schedule arguments for the current term or wait until its next term, which starts in October 2020. If justices decline to hear the case, the challenge will remain with the district court for more analysis about the law’s severability.

Another ACA-related case – Maine Community Health Options v. U.S. – also remains in limbo. Justices heard the case, which was consolidated with two similar challenges, on Dec. 10, 2019, but still have not issued a decision.

The consolidated challenges center on whether the federal government owes insurers billions based on an Affordable Care Act provision intended to help health plans mitigate risk under the law. The ACA’s risk corridor program required the U.S. Department of Health & Human Services to collect funds from profitable insurers that offered qualified health plans under the exchanges and distribute the funds to insurers with excessive losses. Collections from profitable insurers under the program fell short in 2014, 2015, and 2016, while losses steadily grew, resulting in the HHS paying about 12 cents on the dollar in payments to insurers. More than 150 insurers now allege they were shortchanged and they want the Supreme Court to force the government to reimburse them to the tune of $12 billion.

The Department of Justice counters that the government is not required to pay the insurers because of appropriations measures passed by Congress in 2014 and in later years that limited the funding available to compensate insurers for their losses.

The federal government and insurers have each experienced wins and losses at the lower court level. Most recently, the U.S. Court of Appeals for the Federal Circuit decided in favor of the government, ruling that while the ACA required the government to compensate the insurers for their losses, the appropriations measures repealed or suspended that requirement.

A Supreme Court decision in the case could come as soon as Feb. 26.

Court to hear women’s health cases

Two closely watched reproductive health cases will go before the court this spring.

On March 4, justices will hear oral arguments in June Medical Services v. Russo, regarding the constitutionality of a Louisiana law that requires physicians performing abortions to have admitting privileges at a nearby hospital. Doctors who perform abortions without admitting privileges at a hospital within 30 miles face fines and imprisonment, according to the state law, originally passed in 2014. Clinics that employ such doctors can also have their licenses revoked.

June Medical Services LLC, a women’s health clinic, sued over the law. A district court ruled in favor of the plaintiff, but the 5th U.S. Circuit Court of Appeals reversed and upheld Louisiana’s law. The clinic appealed to the U.S. Supreme Court. Louisiana officials argue the challenge should be dismissed, and the law allowed to proceed, because the plaintiffs lack standing.

The Supreme Court in 2016 heard a similar case – Whole Woman’s Health v. Hellerstedt – concerning a comparable law in Texas. In that case, justices struck down the measure as unconstitutional.

And on April 29, justices will hear arguments in Little Sisters of the Poor v. Pennsylvania, a consolidated case about whether the Trump administration acted properly when it expanded exemptions under the Affordable Care Act’s contraceptive mandate. Entities that object to providing contraception on the basis of religious beliefs can opt out of complying with the mandate, according to the 2018 regulations. Additionally, nonprofit organizations and small businesses that have nonreligious moral convictions against the mandate can skip compliance. A number of states and entities sued over the new rules.

A federal appeals court temporarily barred the regulations from moving forward, ruling the plaintiffs were likely to succeed in proving the Trump administration did not follow appropriate procedures when it promulgated the new rules and that the regulations were not authorized under the ACA.

Justices will decide whether the parties have standing in the case, whether the Trump administration followed correct rule-making procedures, and if the regulations can stand.

[email protected]

The Trump administration can move forward with expanding a rule that makes it more difficult for immigrants to remain in the United States if they receive health care assistance, the U.S. Supreme Court ruled in a 5-4 vote.

Courtesy Fred Schilling, Collection of the Supreme Court of the United States

The Feb. 21 order allows the administration to broaden the so-called “public charge rule” while legal challenges against the expanded regulation continue in the lower courts. The Supreme Court’s decision, which lifts a preliminary injunction against the expansion, applies to enforcement only in Illinois, where a district court blocked the revised rule from moving forward in October 2019. The Supreme Court’s measure follows another 5-4 order in January, in which justices lifted a nationwide injunction against the revised rule.

Under the long-standing public charge rule, immigration officials can refuse to admit immigrants into the United States or can deny them permanent legal status if they are deemed likely to become a public charge. Previously, immigration officers considered cash aid, such as Temporary Assistance for Needy Families or long-term institutionalized care, as potential public charge reasons for denial.

The revised regulation allows officials to consider previously excluded programs in their determination, including nonemergency Medicaid, the Supplemental Nutrition Assistance Program, and several housing programs. Use of these programs for more than 12 months in the aggregate during a 36-month period may result in a “public charge” designation and lead to green card denial.

Eight legal challenges were immediately filed against the rule changes, including a complaint issued by 14 states. At least five trial courts have since blocked the measure, while appeals courts have lifted some of the injunctions and upheld enforcement.

In its Jan. 27 order lifting the nationwide injunction, Associate Justice Neil M. Gorsuch wrote that nationwide injunctions are being overused by trial courts with negative consequences.

“The real problem here is the increasingly common practice of trial courts ordering relief that transcends the cases before them. Whether framed as injunctions of ‘nationwide,’ ‘universal,’ or ‘cosmic’ scope, these orders share the same basic flaw – they direct how the defendant must act toward persons who are not parties to the case,” he wrote. “It has become increasingly apparent that this court must, at some point, confront these important objections to this increasingly widespread practice. As the brief and furious history of the regulation before us illustrates, the routine issuance of universal injunctions is patently unworkable, sowing chaos for litigants, the government, courts, and all those affected by these conflicting decisions.”

In the court’s Feb. 21 order lifting the injunction in Illinois, justices gave no explanation for overturning the lower court’s injunction. However, Associate Justice Sonia Sotomayor issued a sharply-worded dissent, criticizing her fellow justices for allowing the rule to proceed.

“In sum, the government’s only claimed hardship is that it must enforce an existing interpretation of an immigration rule in one state – just as it has done for the past 20 years – while an updated version of the rule takes effect in the remaining 49,” she wrote. “The government has not quantified or explained any burdens that would arise from this state of the world.”

ACA cases still in limbo

Meanwhile, the Supreme Court still has not decided whether it will hear Texas v. United States, a case that could effectively dismantle the Affordable Care Act.

The high court was expected to announce whether it would take the high-profile case at a private Feb. 21 conference, but the justices have released no update. The case was relisted for consideration at the court’s Feb. 28 conference.

Texas v. United States stems from a lawsuit by 20 Republican state attorneys general and governors that was filed after Congress zeroed out the ACA’s individual mandate penalty in 2017. The plaintiffs contend the now-valueless mandate is no longer constitutional and thus, the entire ACA should be struck down. Because the Trump administration declined to defend the law, a coalition of Democratic attorneys general and governors intervened in the case as defendants.

In 2018, a Texas district court ruled in favor of the plaintiffs and declared the entire health care law invalid. The 5th U.S. Circuit Court of Appeals partially affirmed the district court’s decision, ruling that the mandate was unconstitutional, but sending the case back to the lower court for more analysis on severability. The Democratic attorneys general and governors appealed the decision to the U.S. Supreme Court.

If the Supreme Court agrees to hear the challenge, the court could fast-track the case and schedule arguments for the current term or wait until its next term, which starts in October 2020. If justices decline to hear the case, the challenge will remain with the district court for more analysis about the law’s severability.

Another ACA-related case – Maine Community Health Options v. U.S. – also remains in limbo. Justices heard the case, which was consolidated with two similar challenges, on Dec. 10, 2019, but still have not issued a decision.

The consolidated challenges center on whether the federal government owes insurers billions based on an Affordable Care Act provision intended to help health plans mitigate risk under the law. The ACA’s risk corridor program required the U.S. Department of Health & Human Services to collect funds from profitable insurers that offered qualified health plans under the exchanges and distribute the funds to insurers with excessive losses. Collections from profitable insurers under the program fell short in 2014, 2015, and 2016, while losses steadily grew, resulting in the HHS paying about 12 cents on the dollar in payments to insurers. More than 150 insurers now allege they were shortchanged and they want the Supreme Court to force the government to reimburse them to the tune of $12 billion.

The Department of Justice counters that the government is not required to pay the insurers because of appropriations measures passed by Congress in 2014 and in later years that limited the funding available to compensate insurers for their losses.

The federal government and insurers have each experienced wins and losses at the lower court level. Most recently, the U.S. Court of Appeals for the Federal Circuit decided in favor of the government, ruling that while the ACA required the government to compensate the insurers for their losses, the appropriations measures repealed or suspended that requirement.

A Supreme Court decision in the case could come as soon as Feb. 26.

Court to hear women’s health cases

Two closely watched reproductive health cases will go before the court this spring.

On March 4, justices will hear oral arguments in June Medical Services v. Russo, regarding the constitutionality of a Louisiana law that requires physicians performing abortions to have admitting privileges at a nearby hospital. Doctors who perform abortions without admitting privileges at a hospital within 30 miles face fines and imprisonment, according to the state law, originally passed in 2014. Clinics that employ such doctors can also have their licenses revoked.

June Medical Services LLC, a women’s health clinic, sued over the law. A district court ruled in favor of the plaintiff, but the 5th U.S. Circuit Court of Appeals reversed and upheld Louisiana’s law. The clinic appealed to the U.S. Supreme Court. Louisiana officials argue the challenge should be dismissed, and the law allowed to proceed, because the plaintiffs lack standing.

The Supreme Court in 2016 heard a similar case – Whole Woman’s Health v. Hellerstedt – concerning a comparable law in Texas. In that case, justices struck down the measure as unconstitutional.

And on April 29, justices will hear arguments in Little Sisters of the Poor v. Pennsylvania, a consolidated case about whether the Trump administration acted properly when it expanded exemptions under the Affordable Care Act’s contraceptive mandate. Entities that object to providing contraception on the basis of religious beliefs can opt out of complying with the mandate, according to the 2018 regulations. Additionally, nonprofit organizations and small businesses that have nonreligious moral convictions against the mandate can skip compliance. A number of states and entities sued over the new rules.

A federal appeals court temporarily barred the regulations from moving forward, ruling the plaintiffs were likely to succeed in proving the Trump administration did not follow appropriate procedures when it promulgated the new rules and that the regulations were not authorized under the ACA.

Justices will decide whether the parties have standing in the case, whether the Trump administration followed correct rule-making procedures, and if the regulations can stand.

[email protected]

It’s past time to call the novel coronavirus, COVID-19, a pandemic and “time to push people to prepare, and guide their prep,” according to risk communication experts.

Courtesy NIAID-RML

Medical messaging about containing or stopping the spread of the virus is doing more harm than good, write Peter Sandman, PhD, and Jody Lanard, MD, both based in New York City, in a recent blog post.

“We are near-certain that the desperate-sounding last-ditch containment messaging of recent days is contributing to a massive global misperception,” they warn.

“The most crucial (and overdue) risk communication task … is to help people visualize their communities when ‘keeping it out’ – containment – is no longer relevant.”

That message is embraced by several experts who spoke to Medscape Medical News.

“I’m jealous of what [they] have written: It is so clear, so correct, and so practical,” said David Fisman, MD, MPH, professor of epidemiology at the University of Toronto, Canada. “I think WHO [World Health Organization] is shying away from the P word,” he continued, referring to the organization’s continuing decision not to call the outbreak a pandemic.

“I fully support exactly what [Sandman and Lanard] are saying,” said Michael Osterholm, PhD, MPH, professor of environmental health sciences and director of the Center for Infectious Disease Research and Policy (CIDRAP) at the University of Minnesota in Minneapolis.

Health care professionals should now be advising people how to prepare – yet this is the most neglected message, Sandman and Lanard write. “Hardly any officials are telling civil society and the general public how to get ready for this pandemic.”

Effective communication should inform people of what to expect now, they continue: “[T]he end of most quarantines, travel restrictions, contact tracing, and other measures designed to keep ‘them’ from infecting ‘us,’ and the switch to measures like canceling mass events designed to keep us from infecting each other.”

Among the new messages that should be delivered are things like:

• Stockpiling nonperishable food and prescription meds.
• Considering care of sick family members.
• Cross-training work personnel so one person’s absence won’t derail an organization’s ability to function.

“We hope that governments and healthcare institutions are using this time wisely,” Sandman and Lanard continue. “We know that ordinary citizens are not being asked to do so. In most countries … ordinary citizens have not been asked to prepare. Instead, they have been led to expect that their governments will keep the virus from their doors.”

This article first appeared on Medscape.com.

It’s past time to call the novel coronavirus, COVID-19, a pandemic and “time to push people to prepare, and guide their prep,” according to risk communication experts.

Courtesy NIAID-RML

Medical messaging about containing or stopping the spread of the virus is doing more harm than good, write Peter Sandman, PhD, and Jody Lanard, MD, both based in New York City, in a recent blog post.

“We are near-certain that the desperate-sounding last-ditch containment messaging of recent days is contributing to a massive global misperception,” they warn.

“The most crucial (and overdue) risk communication task … is to help people visualize their communities when ‘keeping it out’ – containment – is no longer relevant.”

That message is embraced by several experts who spoke to Medscape Medical News.

“I’m jealous of what [they] have written: It is so clear, so correct, and so practical,” said David Fisman, MD, MPH, professor of epidemiology at the University of Toronto, Canada. “I think WHO [World Health Organization] is shying away from the P word,” he continued, referring to the organization’s continuing decision not to call the outbreak a pandemic.

“I fully support exactly what [Sandman and Lanard] are saying,” said Michael Osterholm, PhD, MPH, professor of environmental health sciences and director of the Center for Infectious Disease Research and Policy (CIDRAP) at the University of Minnesota in Minneapolis.

Health care professionals should now be advising people how to prepare – yet this is the most neglected message, Sandman and Lanard write. “Hardly any officials are telling civil society and the general public how to get ready for this pandemic.”

Effective communication should inform people of what to expect now, they continue: “[T]he end of most quarantines, travel restrictions, contact tracing, and other measures designed to keep ‘them’ from infecting ‘us,’ and the switch to measures like canceling mass events designed to keep us from infecting each other.”

Among the new messages that should be delivered are things like:

• Stockpiling nonperishable food and prescription meds.
• Considering care of sick family members.
• Cross-training work personnel so one person’s absence won’t derail an organization’s ability to function.

“We hope that governments and healthcare institutions are using this time wisely,” Sandman and Lanard continue. “We know that ordinary citizens are not being asked to do so. In most countries … ordinary citizens have not been asked to prepare. Instead, they have been led to expect that their governments will keep the virus from their doors.”

This article first appeared on Medscape.com.

It’s past time to call the novel coronavirus, COVID-19, a pandemic and “time to push people to prepare, and guide their prep,” according to risk communication experts.

Courtesy NIAID-RML

Medical messaging about containing or stopping the spread of the virus is doing more harm than good, write Peter Sandman, PhD, and Jody Lanard, MD, both based in New York City, in a recent blog post.

“We are near-certain that the desperate-sounding last-ditch containment messaging of recent days is contributing to a massive global misperception,” they warn.

“The most crucial (and overdue) risk communication task … is to help people visualize their communities when ‘keeping it out’ – containment – is no longer relevant.”

That message is embraced by several experts who spoke to Medscape Medical News.

“I’m jealous of what [they] have written: It is so clear, so correct, and so practical,” said David Fisman, MD, MPH, professor of epidemiology at the University of Toronto, Canada. “I think WHO [World Health Organization] is shying away from the P word,” he continued, referring to the organization’s continuing decision not to call the outbreak a pandemic.

“I fully support exactly what [Sandman and Lanard] are saying,” said Michael Osterholm, PhD, MPH, professor of environmental health sciences and director of the Center for Infectious Disease Research and Policy (CIDRAP) at the University of Minnesota in Minneapolis.

Health care professionals should now be advising people how to prepare – yet this is the most neglected message, Sandman and Lanard write. “Hardly any officials are telling civil society and the general public how to get ready for this pandemic.”

Effective communication should inform people of what to expect now, they continue: “[T]he end of most quarantines, travel restrictions, contact tracing, and other measures designed to keep ‘them’ from infecting ‘us,’ and the switch to measures like canceling mass events designed to keep us from infecting each other.”

Among the new messages that should be delivered are things like:

• Stockpiling nonperishable food and prescription meds.
• Considering care of sick family members.
• Cross-training work personnel so one person’s absence won’t derail an organization’s ability to function.

“We hope that governments and healthcare institutions are using this time wisely,” Sandman and Lanard continue. “We know that ordinary citizens are not being asked to do so. In most countries … ordinary citizens have not been asked to prepare. Instead, they have been led to expect that their governments will keep the virus from their doors.”

This article first appeared on Medscape.com.

Outbreaks of coronavirus in a wide range of countries have officials at the Centers for Disease Control and Prevention believing it is now a matter of when, not if, there will be community spread in the United States.

Courtesy NIAID-RML

“We have for many weeks been saying that, while we hope this is not going to be severe, we are planning as if it is,” Nancy Messonnier, MD, director of the National Center for Immunization and Respiratory Diseases at the CDC, said during a Feb. 25, 2020, telebriefing with reporters. “The data over the last week and the spread in other countries has certainly raised our level of concern and raised our level expectation that we are going to have community spread here.”

Dr. Messonnier noted that the coronavirus is now showing signs of community spread without a known source of exposure in a number of countries, including in Hong Kong, Iran, Italy, Japan, Singapore, South Korea, Taiwan, and Thailand. This has now raised the belief that there will be more widespread outbreaks in the United States.

“What we still don’t know is what that will look like,” she said. “As many of you know, we can have community spread in the United States and have it be reasonably mild. We can have community spread in the U.S. and have it be very severe. That is what we don’t completely know yet and we certainly also don’t exactly know when it is going to happen.”

She reiterated the number of actions being taken to slow the potential spread in the United States, including detecting, tracking, and isolating all cases, as well as restricting travel into the United States and issuing travel advisories for countries where coronavirus outbreaks are known.

“We are doing this with the goal of slowing the introduction of this new virus into the U.S. and buying us more time to prepare,” Dr. Messonnier said, noting the containment strategies have been largely successful, though it will be more difficult as more countries experience community spread of the virus.

Dr. Messonnier also reiterated that at this time there are no vaccines and no medicines to treat the coronavirus. She stressed the need to adhere to nonpharmaceutical interventions (NPIs), as they will be “the most important tools in our response to this virus.”

She said the NPIs will vary based on the severity of the outbreak in any given local community and include personal protective measures that individuals can take every day (many of which mirror the recommendations for preventing the spread of the seasonal flu virus), community NPIs that involve social distancing measures designed to keep people away from others, and environmental NPIs such as surface cleaning measures.

CDC’s latest warning comes as parent agency the Department of Health & Human Services is seeking $2.5 billion in funds from Congress to address the coronavirus outbreak.

During a separate press conference on the same day, HHS Secretary Alex Azar noted that there are five major priorities related to those funds, which would be used in the current year, including expansion of surveillance work within the influenza surveillance network; supporting public health preparedness and response for state and local governments; support the development of therapeutics and the development of vaccines; and the purchase of personal protective equipment for national stockpiles.

Anthony S. Fauci, MD, director of the National Institute of Allergy and Infectious Disease at the National Institutes of Health, added during the press conference that vaccine work is in progress and could be ready for phase 1 testing within a month and a half. If all goes well, it would still be at least 12 - 18 months following the completion of a phase 2 trial before it could be produced for mass consumption.

“It is certainly conceivable that this issue with this coronavirus will go well beyond this season into next season,” Dr. Fauci said. “So a vaccine may not solve the problems of the next couple of months, but it certainly would be an important tool that we would have and we will keep you posted on that.”

He also mentioned that NIAID is looking at a number of candidates for therapeutic treatment of coronavirus. He highlighted Gilead’s remdesivir, a nucleotide analog, as one which undergoing two trials – a randomized controlled trial in China and a copy of that trial in Nebraska among patients with the coronavirus who were taken from the Diamond Princess cruise line in Japan.

“I am optimistic that we will at least get an answer if we do have do have a therapy that really is a gamechanger because then we could do something from the standpoint of intervention for those who are sick,” Dr. Fauci said.  

[email protected]

UPDATE: This story was updated 2/25 at 4:51 p.m. ET

Outbreaks of coronavirus in a wide range of countries have officials at the Centers for Disease Control and Prevention believing it is now a matter of when, not if, there will be community spread in the United States.

Courtesy NIAID-RML

“We have for many weeks been saying that, while we hope this is not going to be severe, we are planning as if it is,” Nancy Messonnier, MD, director of the National Center for Immunization and Respiratory Diseases at the CDC, said during a Feb. 25, 2020, telebriefing with reporters. “The data over the last week and the spread in other countries has certainly raised our level of concern and raised our level expectation that we are going to have community spread here.”

Dr. Messonnier noted that the coronavirus is now showing signs of community spread without a known source of exposure in a number of countries, including in Hong Kong, Iran, Italy, Japan, Singapore, South Korea, Taiwan, and Thailand. This has now raised the belief that there will be more widespread outbreaks in the United States.

“What we still don’t know is what that will look like,” she said. “As many of you know, we can have community spread in the United States and have it be reasonably mild. We can have community spread in the U.S. and have it be very severe. That is what we don’t completely know yet and we certainly also don’t exactly know when it is going to happen.”

She reiterated the number of actions being taken to slow the potential spread in the United States, including detecting, tracking, and isolating all cases, as well as restricting travel into the United States and issuing travel advisories for countries where coronavirus outbreaks are known.

“We are doing this with the goal of slowing the introduction of this new virus into the U.S. and buying us more time to prepare,” Dr. Messonnier said, noting the containment strategies have been largely successful, though it will be more difficult as more countries experience community spread of the virus.

Dr. Messonnier also reiterated that at this time there are no vaccines and no medicines to treat the coronavirus. She stressed the need to adhere to nonpharmaceutical interventions (NPIs), as they will be “the most important tools in our response to this virus.”

She said the NPIs will vary based on the severity of the outbreak in any given local community and include personal protective measures that individuals can take every day (many of which mirror the recommendations for preventing the spread of the seasonal flu virus), community NPIs that involve social distancing measures designed to keep people away from others, and environmental NPIs such as surface cleaning measures.

CDC’s latest warning comes as parent agency the Department of Health & Human Services is seeking $2.5 billion in funds from Congress to address the coronavirus outbreak.

During a separate press conference on the same day, HHS Secretary Alex Azar noted that there are five major priorities related to those funds, which would be used in the current year, including expansion of surveillance work within the influenza surveillance network; supporting public health preparedness and response for state and local governments; support the development of therapeutics and the development of vaccines; and the purchase of personal protective equipment for national stockpiles.

Anthony S. Fauci, MD, director of the National Institute of Allergy and Infectious Disease at the National Institutes of Health, added during the press conference that vaccine work is in progress and could be ready for phase 1 testing within a month and a half. If all goes well, it would still be at least 12 - 18 months following the completion of a phase 2 trial before it could be produced for mass consumption.

“It is certainly conceivable that this issue with this coronavirus will go well beyond this season into next season,” Dr. Fauci said. “So a vaccine may not solve the problems of the next couple of months, but it certainly would be an important tool that we would have and we will keep you posted on that.”

He also mentioned that NIAID is looking at a number of candidates for therapeutic treatment of coronavirus. He highlighted Gilead’s remdesivir, a nucleotide analog, as one which undergoing two trials – a randomized controlled trial in China and a copy of that trial in Nebraska among patients with the coronavirus who were taken from the Diamond Princess cruise line in Japan.

“I am optimistic that we will at least get an answer if we do have do have a therapy that really is a gamechanger because then we could do something from the standpoint of intervention for those who are sick,” Dr. Fauci said.  

[email protected]

UPDATE: This story was updated 2/25 at 4:51 p.m. ET

Outbreaks of coronavirus in a wide range of countries have officials at the Centers for Disease Control and Prevention believing it is now a matter of when, not if, there will be community spread in the United States.

Courtesy NIAID-RML

“We have for many weeks been saying that, while we hope this is not going to be severe, we are planning as if it is,” Nancy Messonnier, MD, director of the National Center for Immunization and Respiratory Diseases at the CDC, said during a Feb. 25, 2020, telebriefing with reporters. “The data over the last week and the spread in other countries has certainly raised our level of concern and raised our level expectation that we are going to have community spread here.”

Dr. Messonnier noted that the coronavirus is now showing signs of community spread without a known source of exposure in a number of countries, including in Hong Kong, Iran, Italy, Japan, Singapore, South Korea, Taiwan, and Thailand. This has now raised the belief that there will be more widespread outbreaks in the United States.

“What we still don’t know is what that will look like,” she said. “As many of you know, we can have community spread in the United States and have it be reasonably mild. We can have community spread in the U.S. and have it be very severe. That is what we don’t completely know yet and we certainly also don’t exactly know when it is going to happen.”

She reiterated the number of actions being taken to slow the potential spread in the United States, including detecting, tracking, and isolating all cases, as well as restricting travel into the United States and issuing travel advisories for countries where coronavirus outbreaks are known.

“We are doing this with the goal of slowing the introduction of this new virus into the U.S. and buying us more time to prepare,” Dr. Messonnier said, noting the containment strategies have been largely successful, though it will be more difficult as more countries experience community spread of the virus.

Dr. Messonnier also reiterated that at this time there are no vaccines and no medicines to treat the coronavirus. She stressed the need to adhere to nonpharmaceutical interventions (NPIs), as they will be “the most important tools in our response to this virus.”

She said the NPIs will vary based on the severity of the outbreak in any given local community and include personal protective measures that individuals can take every day (many of which mirror the recommendations for preventing the spread of the seasonal flu virus), community NPIs that involve social distancing measures designed to keep people away from others, and environmental NPIs such as surface cleaning measures.

CDC’s latest warning comes as parent agency the Department of Health & Human Services is seeking $2.5 billion in funds from Congress to address the coronavirus outbreak.

During a separate press conference on the same day, HHS Secretary Alex Azar noted that there are five major priorities related to those funds, which would be used in the current year, including expansion of surveillance work within the influenza surveillance network; supporting public health preparedness and response for state and local governments; support the development of therapeutics and the development of vaccines; and the purchase of personal protective equipment for national stockpiles.

Anthony S. Fauci, MD, director of the National Institute of Allergy and Infectious Disease at the National Institutes of Health, added during the press conference that vaccine work is in progress and could be ready for phase 1 testing within a month and a half. If all goes well, it would still be at least 12 - 18 months following the completion of a phase 2 trial before it could be produced for mass consumption.

“It is certainly conceivable that this issue with this coronavirus will go well beyond this season into next season,” Dr. Fauci said. “So a vaccine may not solve the problems of the next couple of months, but it certainly would be an important tool that we would have and we will keep you posted on that.”

He also mentioned that NIAID is looking at a number of candidates for therapeutic treatment of coronavirus. He highlighted Gilead’s remdesivir, a nucleotide analog, as one which undergoing two trials – a randomized controlled trial in China and a copy of that trial in Nebraska among patients with the coronavirus who were taken from the Diamond Princess cruise line in Japan.

“I am optimistic that we will at least get an answer if we do have do have a therapy that really is a gamechanger because then we could do something from the standpoint of intervention for those who are sick,” Dr. Fauci said.  

[email protected]

UPDATE: This story was updated 2/25 at 4:51 p.m. ET

There is no Baby Book of Names or hurricane alphabet to readily name diseases and their causal entities. Throughout history and even in the modern era, a host of considerations have intruded on the decision as to what to call these blights upon humanity. Names have varied from inflammatory to misleading, from colloquial to scientific. And when it concerns a new epidemiological entity such as the latest coronavirus outbreak originating in China, health organizations, media, politicians, scientific taxonomy commissions, and the public at large all have a stake in the naming.

Courtesy NIAID-RML

From “Wuhan virus” to “novel coronavirus-2019” to “COVID-19 virus,” the name of the new coronavirus that first appeared in China has been evolving to its now official designation: SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2). But where did the final name come from, how does such a name become official, and who makes it so?
 

Virus taxonomy

The Coronavirus Study Group (CSG) of the International Committee on Taxonomy of Viruses (ICTV) named the new coronavirus SARS-CoV-2 based upon its genetic relationship to the original SARS-CoV that caused an outbreak of disease in 2002–2003.

According to the ICTV website, the first internationally organized attempts to introduce order into the bewildering variety of viruses took place at the International Congress of Microbiology held in Moscow in 1966 where a committee was created that later became the ICTV and was given the task of developing a single, universal taxonomic scheme for all the viruses infecting animals, plants, fungi, bacteria, and archaea. The ICTV was created as a committee of the virology division of the International Union of Microbiological Societies and is governed by statutes approved by the virology division. Virus classification and nomenclature are subject to rules set out in an International Code.

These designate that: “The universal virus classification system shall employ the hierarchical levels of realm, subrealm, kingdom, subkingdom, phylum, subphylum, class, subclass, order, suborder, family, subfamily, genus, subgenus and species.”

Many of the topmost areas of classification are based on whether the viruses are DNA or RNA, single or double stranded, and have a simple protein shell or a complex lipoprotein envelope. Other levels of classification include host species, type of replication, and type of diseases they cause, the later exemplified in the SARS designation for this virus.

There are 98 international study groups (SGs) covering all major virus orders, families, and genera that are part of the ICTV, and it was the one dedicated to the single-stranded RNA coronaviruses, the CSG, that came up with the SARS-CoV-2 name and first referenced it in their Feb 11 publication in the Cold Springs Harbor preprint journal bioRxiv.

“Based on phylogeny, taxonomy and established practice, the CSG formally recognizes this virus as a sister to severe acute respiratory syndrome coronaviruses (SARS-CoVs) of the species severe acute respiratory syndrome–related coronavirus and designates it as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2),” they wrote.

According to the National Center for Biotechnology Information Taxonomy Browser, with respect to the original SARS CoV virus, of which this is a relative, the full taxonomic designation is: Viruses, Riboviria, Nidovirales, Cornidovirineae, Coronaviridae, Orthocoronavirinae, Betacoronavirus, Sarbecovirus.
 

The problem with naming names

The World Health Organization currently is not using the official scientific name of the virus, but rather is merely labeling it with regard to the disease: COVID-19, which simply refers to coronavirus disease 2019.

They are following a modern standard by which disease names avoid inflammatory connotations with people and places. Too often in the past from syphilis as the “French pox,” the 1918 influenza as the “Spanish flu,” AIDS as the “gay plague,” Middle East Respiratory Syndrome (MERS), and the currently named “WuFlu,” which made an appearance early in the new outbreak and which is symbolic of a sudden wave of anti-Asian, and specifically Chinese, prejudice.

Chinatown districts even in the United States are being affected economically through unwarranted fear associated with the virus. And there have been equivalently virulent outbreaks of hate speech against Asian individuals in places untouched by the new virus.

However, although SARS-CoV-2 as a name avoids such problems, different considerations led the WHO to reject it in its discussions, determining that its use ties it to tightly to the much more deadly SARS-CoV-1 virus in the public mind, risking greater fear and panic, especially in Asia, where SARS-CoV-1 had the biggest impact.

Back in 1896, William Sykes, MD, writing in the first flush of the triumph of germ theory in modern medicine, attempted to give some guidance to how medical science should best come up with new names of diseases by merging the demands of common parlance with those of taxonomic legitimacy. His “On the Origin and History of Disease-Names,” published in the Lancet, had clearcut advice: “It is vain to attempt to replace a folk name or one widely adopted by the people by a new one deliberately coined by scholars, and this for the following reasons: first, whatever names may be accepted by medical men must be translated by them into the vernacular of their patients, and by a resulting reaction the vernacular name comes to be the commoner one with themselves; and, secondly, there is no continuity or unchangeableness in the terms invented by savants, which are amended, improved upon, and displaced by the next writer on the subject, or, even more absurdly still, by the very inventors themselves in a subsequent publication.”

This is the reason that virus taxonomy provides names based upon unchangeable scientific descriptors of the actual disease causing entity, as illustrated by the decisions of the ICTV. In addition, the genomic sequences being provided by the scientific community are all being organized under the SARS-CoV-2 name and thus are cementing that moniker as the only acceptable scientific one.

Whether the rest of the world universally adopts SARS-CoV-2 as a name is still in question. If the outbreak spreads significantly beyond its current limits, fear and confusion – and simply the need for a more familiar-sounding label – may lead the general public to adopt more colloquial designations than those that science attempts to impose, as Dr. Sykes suggested back in 1896. That remains to be seen.

[email protected]

Mark Lesney is the managing editor of MDedge.com/IDPractioner. He has a PhD in plant virology and a PhD in the history of science, with a focus on the history of biotechnology and medicine. He has served as an adjunct assistant professor of the department of biochemistry and molecular & cellular biology at Georgetown University, Washington.

There is no Baby Book of Names or hurricane alphabet to readily name diseases and their causal entities. Throughout history and even in the modern era, a host of considerations have intruded on the decision as to what to call these blights upon humanity. Names have varied from inflammatory to misleading, from colloquial to scientific. And when it concerns a new epidemiological entity such as the latest coronavirus outbreak originating in China, health organizations, media, politicians, scientific taxonomy commissions, and the public at large all have a stake in the naming.

Courtesy NIAID-RML

From “Wuhan virus” to “novel coronavirus-2019” to “COVID-19 virus,” the name of the new coronavirus that first appeared in China has been evolving to its now official designation: SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2). But where did the final name come from, how does such a name become official, and who makes it so?
 

Virus taxonomy

The Coronavirus Study Group (CSG) of the International Committee on Taxonomy of Viruses (ICTV) named the new coronavirus SARS-CoV-2 based upon its genetic relationship to the original SARS-CoV that caused an outbreak of disease in 2002–2003.

According to the ICTV website, the first internationally organized attempts to introduce order into the bewildering variety of viruses took place at the International Congress of Microbiology held in Moscow in 1966 where a committee was created that later became the ICTV and was given the task of developing a single, universal taxonomic scheme for all the viruses infecting animals, plants, fungi, bacteria, and archaea. The ICTV was created as a committee of the virology division of the International Union of Microbiological Societies and is governed by statutes approved by the virology division. Virus classification and nomenclature are subject to rules set out in an International Code.

These designate that: “The universal virus classification system shall employ the hierarchical levels of realm, subrealm, kingdom, subkingdom, phylum, subphylum, class, subclass, order, suborder, family, subfamily, genus, subgenus and species.”

Many of the topmost areas of classification are based on whether the viruses are DNA or RNA, single or double stranded, and have a simple protein shell or a complex lipoprotein envelope. Other levels of classification include host species, type of replication, and type of diseases they cause, the later exemplified in the SARS designation for this virus.

There are 98 international study groups (SGs) covering all major virus orders, families, and genera that are part of the ICTV, and it was the one dedicated to the single-stranded RNA coronaviruses, the CSG, that came up with the SARS-CoV-2 name and first referenced it in their Feb 11 publication in the Cold Springs Harbor preprint journal bioRxiv.

“Based on phylogeny, taxonomy and established practice, the CSG formally recognizes this virus as a sister to severe acute respiratory syndrome coronaviruses (SARS-CoVs) of the species severe acute respiratory syndrome–related coronavirus and designates it as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2),” they wrote.

According to the National Center for Biotechnology Information Taxonomy Browser, with respect to the original SARS CoV virus, of which this is a relative, the full taxonomic designation is: Viruses, Riboviria, Nidovirales, Cornidovirineae, Coronaviridae, Orthocoronavirinae, Betacoronavirus, Sarbecovirus.
 

The problem with naming names

The World Health Organization currently is not using the official scientific name of the virus, but rather is merely labeling it with regard to the disease: COVID-19, which simply refers to coronavirus disease 2019.

They are following a modern standard by which disease names avoid inflammatory connotations with people and places. Too often in the past from syphilis as the “French pox,” the 1918 influenza as the “Spanish flu,” AIDS as the “gay plague,” Middle East Respiratory Syndrome (MERS), and the currently named “WuFlu,” which made an appearance early in the new outbreak and which is symbolic of a sudden wave of anti-Asian, and specifically Chinese, prejudice.

Chinatown districts even in the United States are being affected economically through unwarranted fear associated with the virus. And there have been equivalently virulent outbreaks of hate speech against Asian individuals in places untouched by the new virus.

However, although SARS-CoV-2 as a name avoids such problems, different considerations led the WHO to reject it in its discussions, determining that its use ties it to tightly to the much more deadly SARS-CoV-1 virus in the public mind, risking greater fear and panic, especially in Asia, where SARS-CoV-1 had the biggest impact.

Back in 1896, William Sykes, MD, writing in the first flush of the triumph of germ theory in modern medicine, attempted to give some guidance to how medical science should best come up with new names of diseases by merging the demands of common parlance with those of taxonomic legitimacy. His “On the Origin and History of Disease-Names,” published in the Lancet, had clearcut advice: “It is vain to attempt to replace a folk name or one widely adopted by the people by a new one deliberately coined by scholars, and this for the following reasons: first, whatever names may be accepted by medical men must be translated by them into the vernacular of their patients, and by a resulting reaction the vernacular name comes to be the commoner one with themselves; and, secondly, there is no continuity or unchangeableness in the terms invented by savants, which are amended, improved upon, and displaced by the next writer on the subject, or, even more absurdly still, by the very inventors themselves in a subsequent publication.”

This is the reason that virus taxonomy provides names based upon unchangeable scientific descriptors of the actual disease causing entity, as illustrated by the decisions of the ICTV. In addition, the genomic sequences being provided by the scientific community are all being organized under the SARS-CoV-2 name and thus are cementing that moniker as the only acceptable scientific one.

Whether the rest of the world universally adopts SARS-CoV-2 as a name is still in question. If the outbreak spreads significantly beyond its current limits, fear and confusion – and simply the need for a more familiar-sounding label – may lead the general public to adopt more colloquial designations than those that science attempts to impose, as Dr. Sykes suggested back in 1896. That remains to be seen.

[email protected]

Mark Lesney is the managing editor of MDedge.com/IDPractioner. He has a PhD in plant virology and a PhD in the history of science, with a focus on the history of biotechnology and medicine. He has served as an adjunct assistant professor of the department of biochemistry and molecular & cellular biology at Georgetown University, Washington.

There is no Baby Book of Names or hurricane alphabet to readily name diseases and their causal entities. Throughout history and even in the modern era, a host of considerations have intruded on the decision as to what to call these blights upon humanity. Names have varied from inflammatory to misleading, from colloquial to scientific. And when it concerns a new epidemiological entity such as the latest coronavirus outbreak originating in China, health organizations, media, politicians, scientific taxonomy commissions, and the public at large all have a stake in the naming.

Courtesy NIAID-RML

From “Wuhan virus” to “novel coronavirus-2019” to “COVID-19 virus,” the name of the new coronavirus that first appeared in China has been evolving to its now official designation: SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2). But where did the final name come from, how does such a name become official, and who makes it so?
 

Virus taxonomy

The Coronavirus Study Group (CSG) of the International Committee on Taxonomy of Viruses (ICTV) named the new coronavirus SARS-CoV-2 based upon its genetic relationship to the original SARS-CoV that caused an outbreak of disease in 2002–2003.

According to the ICTV website, the first internationally organized attempts to introduce order into the bewildering variety of viruses took place at the International Congress of Microbiology held in Moscow in 1966 where a committee was created that later became the ICTV and was given the task of developing a single, universal taxonomic scheme for all the viruses infecting animals, plants, fungi, bacteria, and archaea. The ICTV was created as a committee of the virology division of the International Union of Microbiological Societies and is governed by statutes approved by the virology division. Virus classification and nomenclature are subject to rules set out in an International Code.

These designate that: “The universal virus classification system shall employ the hierarchical levels of realm, subrealm, kingdom, subkingdom, phylum, subphylum, class, subclass, order, suborder, family, subfamily, genus, subgenus and species.”

Many of the topmost areas of classification are based on whether the viruses are DNA or RNA, single or double stranded, and have a simple protein shell or a complex lipoprotein envelope. Other levels of classification include host species, type of replication, and type of diseases they cause, the later exemplified in the SARS designation for this virus.

There are 98 international study groups (SGs) covering all major virus orders, families, and genera that are part of the ICTV, and it was the one dedicated to the single-stranded RNA coronaviruses, the CSG, that came up with the SARS-CoV-2 name and first referenced it in their Feb 11 publication in the Cold Springs Harbor preprint journal bioRxiv.

“Based on phylogeny, taxonomy and established practice, the CSG formally recognizes this virus as a sister to severe acute respiratory syndrome coronaviruses (SARS-CoVs) of the species severe acute respiratory syndrome–related coronavirus and designates it as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2),” they wrote.

According to the National Center for Biotechnology Information Taxonomy Browser, with respect to the original SARS CoV virus, of which this is a relative, the full taxonomic designation is: Viruses, Riboviria, Nidovirales, Cornidovirineae, Coronaviridae, Orthocoronavirinae, Betacoronavirus, Sarbecovirus.
 

The problem with naming names

The World Health Organization currently is not using the official scientific name of the virus, but rather is merely labeling it with regard to the disease: COVID-19, which simply refers to coronavirus disease 2019.

They are following a modern standard by which disease names avoid inflammatory connotations with people and places. Too often in the past from syphilis as the “French pox,” the 1918 influenza as the “Spanish flu,” AIDS as the “gay plague,” Middle East Respiratory Syndrome (MERS), and the currently named “WuFlu,” which made an appearance early in the new outbreak and which is symbolic of a sudden wave of anti-Asian, and specifically Chinese, prejudice.

Chinatown districts even in the United States are being affected economically through unwarranted fear associated with the virus. And there have been equivalently virulent outbreaks of hate speech against Asian individuals in places untouched by the new virus.

However, although SARS-CoV-2 as a name avoids such problems, different considerations led the WHO to reject it in its discussions, determining that its use ties it to tightly to the much more deadly SARS-CoV-1 virus in the public mind, risking greater fear and panic, especially in Asia, where SARS-CoV-1 had the biggest impact.

Back in 1896, William Sykes, MD, writing in the first flush of the triumph of germ theory in modern medicine, attempted to give some guidance to how medical science should best come up with new names of diseases by merging the demands of common parlance with those of taxonomic legitimacy. His “On the Origin and History of Disease-Names,” published in the Lancet, had clearcut advice: “It is vain to attempt to replace a folk name or one widely adopted by the people by a new one deliberately coined by scholars, and this for the following reasons: first, whatever names may be accepted by medical men must be translated by them into the vernacular of their patients, and by a resulting reaction the vernacular name comes to be the commoner one with themselves; and, secondly, there is no continuity or unchangeableness in the terms invented by savants, which are amended, improved upon, and displaced by the next writer on the subject, or, even more absurdly still, by the very inventors themselves in a subsequent publication.”

This is the reason that virus taxonomy provides names based upon unchangeable scientific descriptors of the actual disease causing entity, as illustrated by the decisions of the ICTV. In addition, the genomic sequences being provided by the scientific community are all being organized under the SARS-CoV-2 name and thus are cementing that moniker as the only acceptable scientific one.

Whether the rest of the world universally adopts SARS-CoV-2 as a name is still in question. If the outbreak spreads significantly beyond its current limits, fear and confusion – and simply the need for a more familiar-sounding label – may lead the general public to adopt more colloquial designations than those that science attempts to impose, as Dr. Sykes suggested back in 1896. That remains to be seen.

[email protected]

Mark Lesney is the managing editor of MDedge.com/IDPractioner. He has a PhD in plant virology and a PhD in the history of science, with a focus on the history of biotechnology and medicine. He has served as an adjunct assistant professor of the department of biochemistry and molecular & cellular biology at Georgetown University, Washington.

MAUI, HAWAII – There might well be a cure for hepatitis B in coming years, just like there is now for hepatitis C, according to Norah Terrault, MD, chief of the division of GI and liver at the University of Southern California, Los Angeles.

M. Alexander Otto/MDedge News

“We are going to have a laundry list of new drugs” that are in the pipeline now. Phase 2 results “look encouraging. You will hear much more about this in the years ahead,” said Dr. Terrault, lead author of the 2018 American Association for the Study of Liver Diseases (AASLD) hepatitis B guidance.

For now, though, the field is largely limited to the nucleoside analogues tenofovir and entecavir. Treatment is often indefinite because, although hepatitis B virus (HBV) e-antigen is cleared, it usually doesn’t clear the HBV surface antigen, which is linked to liver cancer. “Even with e-antigen–negative patients, we feel that indefinite therapy is really the way to go,” Dr. Terrault said at the Gastroenterology Updates, IBD, Liver Disease Conference.

One of the biggest problems with that strategy is what to do when HBV does not seem to be much of a problem for carriers. Such patients are referred to as immune tolerant.
 

A newly recognized cancer risk

Immune tolerant patients tend to be young and have extremely high viral loads but no apparent ill effects, with normal ALT levels, normal histology, and no sign of cirrhosis. Although the AASLD recommends not treating these patients until they are 40 years old, waiting makes people nervous. “You have a hammer, you want to hit a nail,” Dr. Terrault said.

A recent review (Gut. 2018 May;67[5]:945-52) suggests that hitting the nail might be the way to go. South Korean investigators found that 413 untreated immune tolerate patients with a mean age of 38 years had more than twice the risk of liver cancer over 10 years than did almost 1,500 treated patients with active disease.

The study investigators concluded that “unnecessary deaths could be prevented through earlier antiviral intervention in select [immune tolerate] patients.”

This finding is one reason “we [AASLD] are rethinking the mantra of not treating the immune tolerant. There is a group that is transitioning” to active disease. “I’m thinking we should really [lower] the age cutoff” to 30 years, as some other groups [European Association for the Study of the Liver and Asian Pacific Association for the Study of the Liver] have done, plus “patients feel really good when they know the virus is controlled, and so do physicians,” Dr. Terrault said.
 

Entecavir versus tenofovir

Meanwhile, recent studies have raised the question of whether tenofovir is better than entecavir at preventing liver cancer.

A JAMA Oncology (JAMA Oncol. 2019 Jan 1;5[1]:30-6) study of some 25,000 patients in South Korea found a 32% lower risk of liver cancer when they were treated with tenofovir instead of entecavir. “This led to a lot of concern that maybe we should be moving all our patients to tenofovir,” she said.

Another study, a meta-analysis published earlier this year (Hepatol Int. 2020 Jan;14[1]:105-14), confirmed the difference in cancer risk when it combined those findings with other research. After adjustment for potential confounders, including disease stage and length of follow-up, “the difference disappeared” (hazard ration, 0.87; 95% confidence interval, 0.73-1.04), authors of the meta-analysis reported.

Study patients who received entecavir tended to be “treated many years ago and tended to have more severe [baseline] disease,” Dr. Terrault said.

So “while we see this difference, there’s not enough data yet for us to make a recommendation for our patients to switch from” entecavir to tenofovir. “Until a randomized controlled trial is done, this may remain an issue,” she said.
 

A drug holiday?

Dr. Terrault also reviewed research that suggests nucleoside analogue treatment can be stopped in e-antigen–negative patients after at least 3 years.

“The evidence is increasing that a finite NA [nucleoside analogue] treatment approach leads to higher HBsAg [hepatitis B surface antigen] loss rates, compared with the current long-term NA strategy, and can be considered a rational strategy to induce a functional cure in selected HBeAg-negative patients without cirrhosis who are willing to comply with close follow-up monitoring. ... The current observed functional cure rates” – perhaps about 40% – “would be well worth the effort,” editorialists commenting on the research concluded (Hepatology. 2018 Aug;68[2]:397-400).

It’s an interesting idea, Dr. Terrault said, but the virus will flare 8-12 weeks after treatment withdrawal, which is why it shouldn’t be considered in patients with cirrhosis.

Dr. Terrault is a consultant for AbbVie, Merck, Gilead, and other companies and disclosed grants from those companies and others.

[email protected]

MAUI, HAWAII – There might well be a cure for hepatitis B in coming years, just like there is now for hepatitis C, according to Norah Terrault, MD, chief of the division of GI and liver at the University of Southern California, Los Angeles.

M. Alexander Otto/MDedge News

“We are going to have a laundry list of new drugs” that are in the pipeline now. Phase 2 results “look encouraging. You will hear much more about this in the years ahead,” said Dr. Terrault, lead author of the 2018 American Association for the Study of Liver Diseases (AASLD) hepatitis B guidance.

For now, though, the field is largely limited to the nucleoside analogues tenofovir and entecavir. Treatment is often indefinite because, although hepatitis B virus (HBV) e-antigen is cleared, it usually doesn’t clear the HBV surface antigen, which is linked to liver cancer. “Even with e-antigen–negative patients, we feel that indefinite therapy is really the way to go,” Dr. Terrault said at the Gastroenterology Updates, IBD, Liver Disease Conference.

One of the biggest problems with that strategy is what to do when HBV does not seem to be much of a problem for carriers. Such patients are referred to as immune tolerant.
 

A newly recognized cancer risk

Immune tolerant patients tend to be young and have extremely high viral loads but no apparent ill effects, with normal ALT levels, normal histology, and no sign of cirrhosis. Although the AASLD recommends not treating these patients until they are 40 years old, waiting makes people nervous. “You have a hammer, you want to hit a nail,” Dr. Terrault said.

A recent review (Gut. 2018 May;67[5]:945-52) suggests that hitting the nail might be the way to go. South Korean investigators found that 413 untreated immune tolerate patients with a mean age of 38 years had more than twice the risk of liver cancer over 10 years than did almost 1,500 treated patients with active disease.

The study investigators concluded that “unnecessary deaths could be prevented through earlier antiviral intervention in select [immune tolerate] patients.”

This finding is one reason “we [AASLD] are rethinking the mantra of not treating the immune tolerant. There is a group that is transitioning” to active disease. “I’m thinking we should really [lower] the age cutoff” to 30 years, as some other groups [European Association for the Study of the Liver and Asian Pacific Association for the Study of the Liver] have done, plus “patients feel really good when they know the virus is controlled, and so do physicians,” Dr. Terrault said.
 

Entecavir versus tenofovir

Meanwhile, recent studies have raised the question of whether tenofovir is better than entecavir at preventing liver cancer.

A JAMA Oncology (JAMA Oncol. 2019 Jan 1;5[1]:30-6) study of some 25,000 patients in South Korea found a 32% lower risk of liver cancer when they were treated with tenofovir instead of entecavir. “This led to a lot of concern that maybe we should be moving all our patients to tenofovir,” she said.

Another study, a meta-analysis published earlier this year (Hepatol Int. 2020 Jan;14[1]:105-14), confirmed the difference in cancer risk when it combined those findings with other research. After adjustment for potential confounders, including disease stage and length of follow-up, “the difference disappeared” (hazard ration, 0.87; 95% confidence interval, 0.73-1.04), authors of the meta-analysis reported.

Study patients who received entecavir tended to be “treated many years ago and tended to have more severe [baseline] disease,” Dr. Terrault said.

So “while we see this difference, there’s not enough data yet for us to make a recommendation for our patients to switch from” entecavir to tenofovir. “Until a randomized controlled trial is done, this may remain an issue,” she said.
 

A drug holiday?

Dr. Terrault also reviewed research that suggests nucleoside analogue treatment can be stopped in e-antigen–negative patients after at least 3 years.

“The evidence is increasing that a finite NA [nucleoside analogue] treatment approach leads to higher HBsAg [hepatitis B surface antigen] loss rates, compared with the current long-term NA strategy, and can be considered a rational strategy to induce a functional cure in selected HBeAg-negative patients without cirrhosis who are willing to comply with close follow-up monitoring. ... The current observed functional cure rates” – perhaps about 40% – “would be well worth the effort,” editorialists commenting on the research concluded (Hepatology. 2018 Aug;68[2]:397-400).

It’s an interesting idea, Dr. Terrault said, but the virus will flare 8-12 weeks after treatment withdrawal, which is why it shouldn’t be considered in patients with cirrhosis.

Dr. Terrault is a consultant for AbbVie, Merck, Gilead, and other companies and disclosed grants from those companies and others.

[email protected]

MAUI, HAWAII – There might well be a cure for hepatitis B in coming years, just like there is now for hepatitis C, according to Norah Terrault, MD, chief of the division of GI and liver at the University of Southern California, Los Angeles.

M. Alexander Otto/MDedge News

“We are going to have a laundry list of new drugs” that are in the pipeline now. Phase 2 results “look encouraging. You will hear much more about this in the years ahead,” said Dr. Terrault, lead author of the 2018 American Association for the Study of Liver Diseases (AASLD) hepatitis B guidance.

For now, though, the field is largely limited to the nucleoside analogues tenofovir and entecavir. Treatment is often indefinite because, although hepatitis B virus (HBV) e-antigen is cleared, it usually doesn’t clear the HBV surface antigen, which is linked to liver cancer. “Even with e-antigen–negative patients, we feel that indefinite therapy is really the way to go,” Dr. Terrault said at the Gastroenterology Updates, IBD, Liver Disease Conference.

One of the biggest problems with that strategy is what to do when HBV does not seem to be much of a problem for carriers. Such patients are referred to as immune tolerant.
 

A newly recognized cancer risk

Immune tolerant patients tend to be young and have extremely high viral loads but no apparent ill effects, with normal ALT levels, normal histology, and no sign of cirrhosis. Although the AASLD recommends not treating these patients until they are 40 years old, waiting makes people nervous. “You have a hammer, you want to hit a nail,” Dr. Terrault said.

A recent review (Gut. 2018 May;67[5]:945-52) suggests that hitting the nail might be the way to go. South Korean investigators found that 413 untreated immune tolerate patients with a mean age of 38 years had more than twice the risk of liver cancer over 10 years than did almost 1,500 treated patients with active disease.

The study investigators concluded that “unnecessary deaths could be prevented through earlier antiviral intervention in select [immune tolerate] patients.”

This finding is one reason “we [AASLD] are rethinking the mantra of not treating the immune tolerant. There is a group that is transitioning” to active disease. “I’m thinking we should really [lower] the age cutoff” to 30 years, as some other groups [European Association for the Study of the Liver and Asian Pacific Association for the Study of the Liver] have done, plus “patients feel really good when they know the virus is controlled, and so do physicians,” Dr. Terrault said.
 

Entecavir versus tenofovir

Meanwhile, recent studies have raised the question of whether tenofovir is better than entecavir at preventing liver cancer.

A JAMA Oncology (JAMA Oncol. 2019 Jan 1;5[1]:30-6) study of some 25,000 patients in South Korea found a 32% lower risk of liver cancer when they were treated with tenofovir instead of entecavir. “This led to a lot of concern that maybe we should be moving all our patients to tenofovir,” she said.

Another study, a meta-analysis published earlier this year (Hepatol Int. 2020 Jan;14[1]:105-14), confirmed the difference in cancer risk when it combined those findings with other research. After adjustment for potential confounders, including disease stage and length of follow-up, “the difference disappeared” (hazard ration, 0.87; 95% confidence interval, 0.73-1.04), authors of the meta-analysis reported.

Study patients who received entecavir tended to be “treated many years ago and tended to have more severe [baseline] disease,” Dr. Terrault said.

So “while we see this difference, there’s not enough data yet for us to make a recommendation for our patients to switch from” entecavir to tenofovir. “Until a randomized controlled trial is done, this may remain an issue,” she said.
 

A drug holiday?

Dr. Terrault also reviewed research that suggests nucleoside analogue treatment can be stopped in e-antigen–negative patients after at least 3 years.

“The evidence is increasing that a finite NA [nucleoside analogue] treatment approach leads to higher HBsAg [hepatitis B surface antigen] loss rates, compared with the current long-term NA strategy, and can be considered a rational strategy to induce a functional cure in selected HBeAg-negative patients without cirrhosis who are willing to comply with close follow-up monitoring. ... The current observed functional cure rates” – perhaps about 40% – “would be well worth the effort,” editorialists commenting on the research concluded (Hepatology. 2018 Aug;68[2]:397-400).

It’s an interesting idea, Dr. Terrault said, but the virus will flare 8-12 weeks after treatment withdrawal, which is why it shouldn’t be considered in patients with cirrhosis.

Dr. Terrault is a consultant for AbbVie, Merck, Gilead, and other companies and disclosed grants from those companies and others.

[email protected]

Influenza activity dropped during the week ending Feb. 15, according to the Centers for Disease Control and Prevention. That decline, along with revised data from the 2 previous weeks, suggests that the 2019-2020 season has peaked for the second time. The rate of outpatient visits for influenza-like illness (ILI) came in at 6.1% for the week ending Feb. 15, after two straight weeks at 6.7%, the CDC’s influenza division reported Feb. 21.

The rates for those 2 earlier weeks had previously been reported at 6.8% (Feb. 8) and 6.6% (Feb. 1), which means that there have now been 2 consecutive weeks without an increase in national ILI activity.

State-level activity was down slightly as well. For the week ending Feb. 15, there were 39 states and Puerto Rico at the highest level of activity on the CDC’s 1-10 scale, compared with 41 states and Puerto Rico the week before. The number of states in the “high” range, which includes levels 8 and 9, went from 44 to 45, however, CDC data show.

Laboratory measures also dropped a bit. For the week, 29.6% of respiratory specimens tested positive for influenza, compared with 30.3% the previous week. The predominance of influenza A continued to increase, as type A went from 59.4% to 63.5% of positive specimens and type B dropped from 40.6% to 36.5%, the influenza division said.

In a separate report, the CDC announced interim flu vaccine effectiveness estimates.For the 2019-2020 season so far, “flu vaccines are reducing doctor’s visits for flu illness by almost half (45%). This is consistent with estimates of flu vaccine effectiveness (VE) from previous flu seasons that ranged from 40% to 60% when flu vaccine viruses were similar to circulating influenza viruses,” the CDC said.

Although VE among children aged 6 months to 17 years is even higher, at 55%, this season “has been especially bad for children. Flu hospitalization rates among children are higher than at this time in other recent seasons, including the 2017-18 season,” the CDC noted.

The number of pediatric flu deaths for 2019-2020 – now up to 105 – is “higher for the same time period than in every season since reporting began in 2004-05, with the exception of the 2009 pandemic,” the CDC added.

Interim VE estimates for other age groups are 25% for adults aged 18-49 and 43% for those 50 years and older. “The lower VE point estimates observed among adults 18-49 years appear to be associated with a trend suggesting lower VE in this age group against A(H1N1)pdm09 viruses,” the CDC said.

[email protected]

Influenza activity dropped during the week ending Feb. 15, according to the Centers for Disease Control and Prevention. That decline, along with revised data from the 2 previous weeks, suggests that the 2019-2020 season has peaked for the second time. The rate of outpatient visits for influenza-like illness (ILI) came in at 6.1% for the week ending Feb. 15, after two straight weeks at 6.7%, the CDC’s influenza division reported Feb. 21.

The rates for those 2 earlier weeks had previously been reported at 6.8% (Feb. 8) and 6.6% (Feb. 1), which means that there have now been 2 consecutive weeks without an increase in national ILI activity.

State-level activity was down slightly as well. For the week ending Feb. 15, there were 39 states and Puerto Rico at the highest level of activity on the CDC’s 1-10 scale, compared with 41 states and Puerto Rico the week before. The number of states in the “high” range, which includes levels 8 and 9, went from 44 to 45, however, CDC data show.

Laboratory measures also dropped a bit. For the week, 29.6% of respiratory specimens tested positive for influenza, compared with 30.3% the previous week. The predominance of influenza A continued to increase, as type A went from 59.4% to 63.5% of positive specimens and type B dropped from 40.6% to 36.5%, the influenza division said.

In a separate report, the CDC announced interim flu vaccine effectiveness estimates.For the 2019-2020 season so far, “flu vaccines are reducing doctor’s visits for flu illness by almost half (45%). This is consistent with estimates of flu vaccine effectiveness (VE) from previous flu seasons that ranged from 40% to 60% when flu vaccine viruses were similar to circulating influenza viruses,” the CDC said.

Although VE among children aged 6 months to 17 years is even higher, at 55%, this season “has been especially bad for children. Flu hospitalization rates among children are higher than at this time in other recent seasons, including the 2017-18 season,” the CDC noted.

The number of pediatric flu deaths for 2019-2020 – now up to 105 – is “higher for the same time period than in every season since reporting began in 2004-05, with the exception of the 2009 pandemic,” the CDC added.

Interim VE estimates for other age groups are 25% for adults aged 18-49 and 43% for those 50 years and older. “The lower VE point estimates observed among adults 18-49 years appear to be associated with a trend suggesting lower VE in this age group against A(H1N1)pdm09 viruses,” the CDC said.

[email protected]

Influenza activity dropped during the week ending Feb. 15, according to the Centers for Disease Control and Prevention. That decline, along with revised data from the 2 previous weeks, suggests that the 2019-2020 season has peaked for the second time. The rate of outpatient visits for influenza-like illness (ILI) came in at 6.1% for the week ending Feb. 15, after two straight weeks at 6.7%, the CDC’s influenza division reported Feb. 21.

The rates for those 2 earlier weeks had previously been reported at 6.8% (Feb. 8) and 6.6% (Feb. 1), which means that there have now been 2 consecutive weeks without an increase in national ILI activity.

State-level activity was down slightly as well. For the week ending Feb. 15, there were 39 states and Puerto Rico at the highest level of activity on the CDC’s 1-10 scale, compared with 41 states and Puerto Rico the week before. The number of states in the “high” range, which includes levels 8 and 9, went from 44 to 45, however, CDC data show.

Laboratory measures also dropped a bit. For the week, 29.6% of respiratory specimens tested positive for influenza, compared with 30.3% the previous week. The predominance of influenza A continued to increase, as type A went from 59.4% to 63.5% of positive specimens and type B dropped from 40.6% to 36.5%, the influenza division said.

In a separate report, the CDC announced interim flu vaccine effectiveness estimates.For the 2019-2020 season so far, “flu vaccines are reducing doctor’s visits for flu illness by almost half (45%). This is consistent with estimates of flu vaccine effectiveness (VE) from previous flu seasons that ranged from 40% to 60% when flu vaccine viruses were similar to circulating influenza viruses,” the CDC said.

Although VE among children aged 6 months to 17 years is even higher, at 55%, this season “has been especially bad for children. Flu hospitalization rates among children are higher than at this time in other recent seasons, including the 2017-18 season,” the CDC noted.

The number of pediatric flu deaths for 2019-2020 – now up to 105 – is “higher for the same time period than in every season since reporting began in 2004-05, with the exception of the 2009 pandemic,” the CDC added.

Interim VE estimates for other age groups are 25% for adults aged 18-49 and 43% for those 50 years and older. “The lower VE point estimates observed among adults 18-49 years appear to be associated with a trend suggesting lower VE in this age group against A(H1N1)pdm09 viruses,” the CDC said.

[email protected]

As of 6 a.m. Geneva time, Feb. 21, China reported 75,567 cases of COVID-19 and 2,239 deaths, including a total of 892 new confirmed cases that were reported in China in the past 24 hours, with 118 deaths, stated Tedros Adhanom Ghebreyesus, MD, World Health Organization Director-General, in a Feb. 21 news conference on the COVID-19 outbreak.

What he described as “the significant decline in newly reported cases” is partly because of a change in reporting in which China switched from including “clinically diagnosed” cases to reporting only “suspected” and “laboratory confirmed cases.” The reporting procedure changed because the medical facilities in Wuhan regained the capability of checking all suspected cases with laboratory tests. As a result, some cases that were clinically confirmed were subtracted from the total because they tested negative, said Dr. Ghebreyesus.

Although the number of cases in Hubuei province continues to decline, the WHO is concerned about an increase seen in Shandong province and they are seeking more information. Outside China, there are now 1,152 cases in 26 countries and eight deaths. “Although the number of cases outside of China remains small, we are concerned about the cases with no clear epidemiological link, such as travel history to China, or contact with a confirmed case,” said Dr. Ghebreyesus. “Apart from the Diamond Princess cruise ship, the Republic of Korea now has the most cases outside China, and we are working closely with that government to understand the transmission dynamics that led to this increase.”

“We are also concerned about the increase of cases in the Islamic Republic of Iran, where there are now 18 cases and four deaths in just the past 2 days.”

“Our particular concern is for COVID-19 to spread in countries with weaker health systems,” he said, adding that tomorrow, he will address an emergency meeting of African health ministers held jointly by the African Union and the African Centres for Disease Control and Prevention on dealing with COVID-19.

Dr. Ghebreyesus also announced that today the WHO has designated six special envoys on COVID-19 to provide strategic advice and high-level political advocacy and engagement in different parts of the world.

In his remarks, Dr. Ghebreyesus particularly stressed that: “The measures that China and other countries have taken have given us a fighting chance of containing the spread of the virus. We call on all countries to continue their commitment for containment measures, while preparing for community transmission if it occurs. We must not look back and regret that we failed to take advantage of the window of opportunity that we have now.”

In the question and answer period, Dr. Ghebreyesus specifically addressed the issue of misinformation and conspiracy theories being promulgated by certain individuals and on social media about the source of the virus, especially those people who believe that it was designed in a Chinese virus laboratory. Scientists play an important role in refuting such particular misinformation, he said, and research must continue to track down the actual source in nature.

To that regard, a paper published online in the Lancet on Feb. 19, provided a consensus statement by more than 25 health scientists outside of China stating: “We stand together to strongly condemn conspiracy theories suggesting that COVID-19 does not have a natural origin. Scientists from multiple countries have published and analyzed genomes of the causative agent, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), and they overwhelmingly conclude that this coronavirus originated in wildlife, as have so many other emerging pathogens.”

The WHO issues daily coronavirus disease (COVID-2019) situation reports on its website and provides these telebriefing updates daily.

[email protected]

As of 6 a.m. Geneva time, Feb. 21, China reported 75,567 cases of COVID-19 and 2,239 deaths, including a total of 892 new confirmed cases that were reported in China in the past 24 hours, with 118 deaths, stated Tedros Adhanom Ghebreyesus, MD, World Health Organization Director-General, in a Feb. 21 news conference on the COVID-19 outbreak.

What he described as “the significant decline in newly reported cases” is partly because of a change in reporting in which China switched from including “clinically diagnosed” cases to reporting only “suspected” and “laboratory confirmed cases.” The reporting procedure changed because the medical facilities in Wuhan regained the capability of checking all suspected cases with laboratory tests. As a result, some cases that were clinically confirmed were subtracted from the total because they tested negative, said Dr. Ghebreyesus.

Although the number of cases in Hubuei province continues to decline, the WHO is concerned about an increase seen in Shandong province and they are seeking more information. Outside China, there are now 1,152 cases in 26 countries and eight deaths. “Although the number of cases outside of China remains small, we are concerned about the cases with no clear epidemiological link, such as travel history to China, or contact with a confirmed case,” said Dr. Ghebreyesus. “Apart from the Diamond Princess cruise ship, the Republic of Korea now has the most cases outside China, and we are working closely with that government to understand the transmission dynamics that led to this increase.”

“We are also concerned about the increase of cases in the Islamic Republic of Iran, where there are now 18 cases and four deaths in just the past 2 days.”

“Our particular concern is for COVID-19 to spread in countries with weaker health systems,” he said, adding that tomorrow, he will address an emergency meeting of African health ministers held jointly by the African Union and the African Centres for Disease Control and Prevention on dealing with COVID-19.

Dr. Ghebreyesus also announced that today the WHO has designated six special envoys on COVID-19 to provide strategic advice and high-level political advocacy and engagement in different parts of the world.

In his remarks, Dr. Ghebreyesus particularly stressed that: “The measures that China and other countries have taken have given us a fighting chance of containing the spread of the virus. We call on all countries to continue their commitment for containment measures, while preparing for community transmission if it occurs. We must not look back and regret that we failed to take advantage of the window of opportunity that we have now.”

In the question and answer period, Dr. Ghebreyesus specifically addressed the issue of misinformation and conspiracy theories being promulgated by certain individuals and on social media about the source of the virus, especially those people who believe that it was designed in a Chinese virus laboratory. Scientists play an important role in refuting such particular misinformation, he said, and research must continue to track down the actual source in nature.

To that regard, a paper published online in the Lancet on Feb. 19, provided a consensus statement by more than 25 health scientists outside of China stating: “We stand together to strongly condemn conspiracy theories suggesting that COVID-19 does not have a natural origin. Scientists from multiple countries have published and analyzed genomes of the causative agent, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), and they overwhelmingly conclude that this coronavirus originated in wildlife, as have so many other emerging pathogens.”

The WHO issues daily coronavirus disease (COVID-2019) situation reports on its website and provides these telebriefing updates daily.

[email protected]

As of 6 a.m. Geneva time, Feb. 21, China reported 75,567 cases of COVID-19 and 2,239 deaths, including a total of 892 new confirmed cases that were reported in China in the past 24 hours, with 118 deaths, stated Tedros Adhanom Ghebreyesus, MD, World Health Organization Director-General, in a Feb. 21 news conference on the COVID-19 outbreak.

What he described as “the significant decline in newly reported cases” is partly because of a change in reporting in which China switched from including “clinically diagnosed” cases to reporting only “suspected” and “laboratory confirmed cases.” The reporting procedure changed because the medical facilities in Wuhan regained the capability of checking all suspected cases with laboratory tests. As a result, some cases that were clinically confirmed were subtracted from the total because they tested negative, said Dr. Ghebreyesus.

Although the number of cases in Hubuei province continues to decline, the WHO is concerned about an increase seen in Shandong province and they are seeking more information. Outside China, there are now 1,152 cases in 26 countries and eight deaths. “Although the number of cases outside of China remains small, we are concerned about the cases with no clear epidemiological link, such as travel history to China, or contact with a confirmed case,” said Dr. Ghebreyesus. “Apart from the Diamond Princess cruise ship, the Republic of Korea now has the most cases outside China, and we are working closely with that government to understand the transmission dynamics that led to this increase.”

“We are also concerned about the increase of cases in the Islamic Republic of Iran, where there are now 18 cases and four deaths in just the past 2 days.”

“Our particular concern is for COVID-19 to spread in countries with weaker health systems,” he said, adding that tomorrow, he will address an emergency meeting of African health ministers held jointly by the African Union and the African Centres for Disease Control and Prevention on dealing with COVID-19.

Dr. Ghebreyesus also announced that today the WHO has designated six special envoys on COVID-19 to provide strategic advice and high-level political advocacy and engagement in different parts of the world.

In his remarks, Dr. Ghebreyesus particularly stressed that: “The measures that China and other countries have taken have given us a fighting chance of containing the spread of the virus. We call on all countries to continue their commitment for containment measures, while preparing for community transmission if it occurs. We must not look back and regret that we failed to take advantage of the window of opportunity that we have now.”

In the question and answer period, Dr. Ghebreyesus specifically addressed the issue of misinformation and conspiracy theories being promulgated by certain individuals and on social media about the source of the virus, especially those people who believe that it was designed in a Chinese virus laboratory. Scientists play an important role in refuting such particular misinformation, he said, and research must continue to track down the actual source in nature.

To that regard, a paper published online in the Lancet on Feb. 19, provided a consensus statement by more than 25 health scientists outside of China stating: “We stand together to strongly condemn conspiracy theories suggesting that COVID-19 does not have a natural origin. Scientists from multiple countries have published and analyzed genomes of the causative agent, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), and they overwhelmingly conclude that this coronavirus originated in wildlife, as have so many other emerging pathogens.”

The WHO issues daily coronavirus disease (COVID-2019) situation reports on its website and provides these telebriefing updates daily.

[email protected]

Researchers have identified the structure of a protein that could turn out to be a potential vaccine target for the 2019-nCoV.

Jason McLellan/Univ. of Texas at Austin

As is typical of other coronaviruses, 2019-nCoV makes use of a densely glycosylated spike protein to gain entry into host cells. The spike protein is a trimeric class I fusion protein that exists in a metastable prefusion conformation that undergoes a dramatic structural rearrangement to fuse the viral membrane with the host-cell membrane, according to Daniel Wrapp of the University of Texas at Austin and colleagues.

The researchers performed a study to synthesize and determine the 3-D structure of the spike protein because it is a logical target for vaccine development and for the development of targeted therapeutics for COVID-19, the disease caused by the virus.

“As soon as we knew this was a coronavirus, we felt we had to jump at it,” senior author Jason S. McLellan, PhD, associate professor of molecular science, said in a press release from the University, “because we could be one of the first ones to get this structure. We knew exactly what mutations to put into this because we’ve already shown these mutations work for a bunch of other coronaviruses.”

Because recent reports by other researchers demonstrated that 2019-nCoV and SARS-CoV spike proteins share the same functional host-cell receptor–angiotensin-converting enzyme 2 (ACE2), Dr. McLellan and his colleagues examined the relation between the two viruses. They found biophysical and structural evidence that the 2019-nCoV spike protein binds ACE2 with higher affinity than the closely related SARS-CoV spike protein. “The high affinity of 2019-nCoV S for human ACE2 may contribute to the apparent ease with which 2019-nCoV can spread from human-to-human; however, additional studies are needed to investigate this possibility,” the researchers wrote.

Focusing their attention on the receptor-binding domain (RBD) of the 2019-nCoV spike protein, they tested several published SARS-CoV RBD-specific monoclonal antibodies against it and found that these antibodies showed no appreciable binding to 2019-nCoV spike protein, which suggests limited antibody cross-reactivity. For this reason, they suggested that future antibody isolation and therapeutic design efforts will benefit from specifically using 2019-nCoV spike proteins as probes.

“This information will support precision vaccine design and discovery of anti-viral therapeutics, accelerating medical countermeasure development,” they concluded.

The research was supported in part by an National Institutes of Health/National Institute of Allergy and Infectious Diseases grant and by intramural funding from the National Institute of Allergy and Infectious Diseases. Four authors are inventors on US patent application No. 62/412,703 (Prefusion Coronavirus Spike Proteins and Their Use) and all are inventors on US patent application No. 62/972,886 (2019-nCoV Vaccine).

[email protected]

SOURCE: Wrapp D et al. Science. 2020 Feb 19. doi: 10.1126/science.abb2507.

Researchers have identified the structure of a protein that could turn out to be a potential vaccine target for the 2019-nCoV.

Jason McLellan/Univ. of Texas at Austin

As is typical of other coronaviruses, 2019-nCoV makes use of a densely glycosylated spike protein to gain entry into host cells. The spike protein is a trimeric class I fusion protein that exists in a metastable prefusion conformation that undergoes a dramatic structural rearrangement to fuse the viral membrane with the host-cell membrane, according to Daniel Wrapp of the University of Texas at Austin and colleagues.

The researchers performed a study to synthesize and determine the 3-D structure of the spike protein because it is a logical target for vaccine development and for the development of targeted therapeutics for COVID-19, the disease caused by the virus.

“As soon as we knew this was a coronavirus, we felt we had to jump at it,” senior author Jason S. McLellan, PhD, associate professor of molecular science, said in a press release from the University, “because we could be one of the first ones to get this structure. We knew exactly what mutations to put into this because we’ve already shown these mutations work for a bunch of other coronaviruses.”

Because recent reports by other researchers demonstrated that 2019-nCoV and SARS-CoV spike proteins share the same functional host-cell receptor–angiotensin-converting enzyme 2 (ACE2), Dr. McLellan and his colleagues examined the relation between the two viruses. They found biophysical and structural evidence that the 2019-nCoV spike protein binds ACE2 with higher affinity than the closely related SARS-CoV spike protein. “The high affinity of 2019-nCoV S for human ACE2 may contribute to the apparent ease with which 2019-nCoV can spread from human-to-human; however, additional studies are needed to investigate this possibility,” the researchers wrote.

Focusing their attention on the receptor-binding domain (RBD) of the 2019-nCoV spike protein, they tested several published SARS-CoV RBD-specific monoclonal antibodies against it and found that these antibodies showed no appreciable binding to 2019-nCoV spike protein, which suggests limited antibody cross-reactivity. For this reason, they suggested that future antibody isolation and therapeutic design efforts will benefit from specifically using 2019-nCoV spike proteins as probes.

“This information will support precision vaccine design and discovery of anti-viral therapeutics, accelerating medical countermeasure development,” they concluded.

The research was supported in part by an National Institutes of Health/National Institute of Allergy and Infectious Diseases grant and by intramural funding from the National Institute of Allergy and Infectious Diseases. Four authors are inventors on US patent application No. 62/412,703 (Prefusion Coronavirus Spike Proteins and Their Use) and all are inventors on US patent application No. 62/972,886 (2019-nCoV Vaccine).

[email protected]

SOURCE: Wrapp D et al. Science. 2020 Feb 19. doi: 10.1126/science.abb2507.

Researchers have identified the structure of a protein that could turn out to be a potential vaccine target for the 2019-nCoV.

Jason McLellan/Univ. of Texas at Austin

As is typical of other coronaviruses, 2019-nCoV makes use of a densely glycosylated spike protein to gain entry into host cells. The spike protein is a trimeric class I fusion protein that exists in a metastable prefusion conformation that undergoes a dramatic structural rearrangement to fuse the viral membrane with the host-cell membrane, according to Daniel Wrapp of the University of Texas at Austin and colleagues.

The researchers performed a study to synthesize and determine the 3-D structure of the spike protein because it is a logical target for vaccine development and for the development of targeted therapeutics for COVID-19, the disease caused by the virus.

“As soon as we knew this was a coronavirus, we felt we had to jump at it,” senior author Jason S. McLellan, PhD, associate professor of molecular science, said in a press release from the University, “because we could be one of the first ones to get this structure. We knew exactly what mutations to put into this because we’ve already shown these mutations work for a bunch of other coronaviruses.”

Because recent reports by other researchers demonstrated that 2019-nCoV and SARS-CoV spike proteins share the same functional host-cell receptor–angiotensin-converting enzyme 2 (ACE2), Dr. McLellan and his colleagues examined the relation between the two viruses. They found biophysical and structural evidence that the 2019-nCoV spike protein binds ACE2 with higher affinity than the closely related SARS-CoV spike protein. “The high affinity of 2019-nCoV S for human ACE2 may contribute to the apparent ease with which 2019-nCoV can spread from human-to-human; however, additional studies are needed to investigate this possibility,” the researchers wrote.

Focusing their attention on the receptor-binding domain (RBD) of the 2019-nCoV spike protein, they tested several published SARS-CoV RBD-specific monoclonal antibodies against it and found that these antibodies showed no appreciable binding to 2019-nCoV spike protein, which suggests limited antibody cross-reactivity. For this reason, they suggested that future antibody isolation and therapeutic design efforts will benefit from specifically using 2019-nCoV spike proteins as probes.

“This information will support precision vaccine design and discovery of anti-viral therapeutics, accelerating medical countermeasure development,” they concluded.

The research was supported in part by an National Institutes of Health/National Institute of Allergy and Infectious Diseases grant and by intramural funding from the National Institute of Allergy and Infectious Diseases. Four authors are inventors on US patent application No. 62/412,703 (Prefusion Coronavirus Spike Proteins and Their Use) and all are inventors on US patent application No. 62/972,886 (2019-nCoV Vaccine).

[email protected]

SOURCE: Wrapp D et al. Science. 2020 Feb 19. doi: 10.1126/science.abb2507.

LOS ANGELES – Prevention of shingles with the Zoster Vaccine Live may reduce the risk of subsequent stroke among older adults as well, the first study to examine this association suggests. Shingles vaccination was linked to a 20% decrease in stroke risk in people younger than 80 years of age in the large Medicare cohort study. Older participants showed a 10% reduced risk, according to data released in advance of formal presentation at this week’s International Stroke Conference, sponsored by the American Heart Association.

Reductions were seen for both ischemic and hemorrhagic events.

“Our findings might encourage people age 50 or older to get vaccinated against shingles and to prevent shingles-associated stroke risk,” Quanhe Yang, PhD, lead study author and senior scientist at the Centers for Disease Control and Prevention, said in an interview.

Dr. Yang and colleagues evaluated the only shingles vaccine available at the time of the study, Zoster Vaccine Live (Zostavax). However, the CDC now calls an adjuvanted, nonlive recombinant vaccine (Shingrix) the preferred shingles vaccine for healthy adults aged 50 years and older. Shingrix was approved in 2017. Zostavax, approved in 2006, can still be used in healthy adults aged 60 years and older, the agency states.

A reduction in inflammation from Zoster Vaccine Live may be the mechanism by which stroke risk is reduced, Dr. Yang said. The newer vaccine, which the CDC notes is more than 90% effective, might provide even greater protection against stroke, although more research is needed, he added.

Interestingly, prior research suggested that, once a person develops shingles, it may be too late. Dr. Yang and colleagues showed vaccination or antiviral treatment after a shingles episode was not effective at reducing stroke risk in research presented at the 2019 International Stroke Conference.

Shingles can present as a painful reactivation of chickenpox, also known as the varicella-zoster virus. Shingles is also common; Dr. Yang estimated one in three people who had chickenpox will develop the condition at some point in their lifetime. In addition, researchers have linked shingles to an elevated risk of stroke.

To assess the vaccine’s protective effect on stroke, Dr. Yang and colleagues reviewed health records for 1.38 million Medicare recipients. All participants were aged 66 years or older, had no history of stroke at baseline, and received the Zoster Vaccine Live during 2008-2016. The investigators compared the stroke rate in this vaccinated group with the rate in a matched control group of the same number of Medicare fee-for-service beneficiaries who did not receive the vaccination. They adjusted their analysis for age, sex, race, medications, and comorbidities.

The overall decrease of 16% in stroke risk associated with vaccination included a 12% drop in hemorrhagic stroke and 18% decrease in ischemic stroke over a median follow-up of 3.9 years follow-up (interquartile range, 2.7-5.4).

The adjusted hazard ratios comparing the vaccinated with control groups were 0.84 (95% confidence interval, 0.83-0.85) for all stroke; 0.82 (95% CI, 0.81-0.83) for acute ischemic stroke; and 0.88 (95% CI, 0.84-0.91) for hemorrhagic stroke.

The vaccinated group experienced 42,267 stroke events during that time. This rate included 33,510 acute ischemic strokes and 4,318 hemorrhagic strokes. At the same time, 48,139 strokes occurred in the control group. The breakdown included 39,334 ischemic and 4,713 hemorrhagic events.

“Approximately 1 million people in the United States get shingles each year, yet there is a vaccine to help prevent it,” Dr. Yang stated in a news release. “Our study results may encourage people ages 50 and older to follow the recommendation and get vaccinated against shingles. You are reducing the risk of shingles, and at the same time, you may be reducing your risk of stroke.”

“Further studies are needed to confirm our findings of association between Zostavax vaccine and risk of stroke,” Dr. Yang said.

Because the CDC Advisory Committee on Immunization Practices recommended Shingrix vaccine only for healthy adults 50 years and older in 2017, there were insufficient data in Medicare to study the association between that vaccine and risk of stroke at the time of the current study.

“However, two doses of Shingrix are more than 90% effective at preventing shingles and postherpetic neuralgia, and higher than that of Zostavax,” Dr. Yang said.

‘Very intriguing’ research

“This is a very interesting study,” Ralph L. Sacco, MD, past president of the American Heart Association, said in a video commentary released in advance of the conference. It was a very large sample, he noted, and those older than age 60 years who had the vaccine were protected with a lower risk for both ischemic and hemorrhagic stroke.

“So it is very intriguing,” added Dr. Sacco, chairman of the department of neurology at the University of Miami. “We know things like shingles can increase inflammation and increase the risk of stroke,” Dr. Sacco said, “but this is the first time in a very large Medicare database that it was shown that those who had the vaccine had a lower risk of stroke.”

The CDC funded this study. Dr. Yang and Dr. Sacco have disclosed no relevant financial relationships.

SOURCE: Yang Q et al. ISC 2020, Abstract TP493.

This article first appeared on Medscape.com.

LOS ANGELES – Prevention of shingles with the Zoster Vaccine Live may reduce the risk of subsequent stroke among older adults as well, the first study to examine this association suggests. Shingles vaccination was linked to a 20% decrease in stroke risk in people younger than 80 years of age in the large Medicare cohort study. Older participants showed a 10% reduced risk, according to data released in advance of formal presentation at this week’s International Stroke Conference, sponsored by the American Heart Association.

Reductions were seen for both ischemic and hemorrhagic events.

“Our findings might encourage people age 50 or older to get vaccinated against shingles and to prevent shingles-associated stroke risk,” Quanhe Yang, PhD, lead study author and senior scientist at the Centers for Disease Control and Prevention, said in an interview.

Dr. Yang and colleagues evaluated the only shingles vaccine available at the time of the study, Zoster Vaccine Live (Zostavax). However, the CDC now calls an adjuvanted, nonlive recombinant vaccine (Shingrix) the preferred shingles vaccine for healthy adults aged 50 years and older. Shingrix was approved in 2017. Zostavax, approved in 2006, can still be used in healthy adults aged 60 years and older, the agency states.

A reduction in inflammation from Zoster Vaccine Live may be the mechanism by which stroke risk is reduced, Dr. Yang said. The newer vaccine, which the CDC notes is more than 90% effective, might provide even greater protection against stroke, although more research is needed, he added.

Interestingly, prior research suggested that, once a person develops shingles, it may be too late. Dr. Yang and colleagues showed vaccination or antiviral treatment after a shingles episode was not effective at reducing stroke risk in research presented at the 2019 International Stroke Conference.

Shingles can present as a painful reactivation of chickenpox, also known as the varicella-zoster virus. Shingles is also common; Dr. Yang estimated one in three people who had chickenpox will develop the condition at some point in their lifetime. In addition, researchers have linked shingles to an elevated risk of stroke.

To assess the vaccine’s protective effect on stroke, Dr. Yang and colleagues reviewed health records for 1.38 million Medicare recipients. All participants were aged 66 years or older, had no history of stroke at baseline, and received the Zoster Vaccine Live during 2008-2016. The investigators compared the stroke rate in this vaccinated group with the rate in a matched control group of the same number of Medicare fee-for-service beneficiaries who did not receive the vaccination. They adjusted their analysis for age, sex, race, medications, and comorbidities.

The overall decrease of 16% in stroke risk associated with vaccination included a 12% drop in hemorrhagic stroke and 18% decrease in ischemic stroke over a median follow-up of 3.9 years follow-up (interquartile range, 2.7-5.4).

The adjusted hazard ratios comparing the vaccinated with control groups were 0.84 (95% confidence interval, 0.83-0.85) for all stroke; 0.82 (95% CI, 0.81-0.83) for acute ischemic stroke; and 0.88 (95% CI, 0.84-0.91) for hemorrhagic stroke.

The vaccinated group experienced 42,267 stroke events during that time. This rate included 33,510 acute ischemic strokes and 4,318 hemorrhagic strokes. At the same time, 48,139 strokes occurred in the control group. The breakdown included 39,334 ischemic and 4,713 hemorrhagic events.

“Approximately 1 million people in the United States get shingles each year, yet there is a vaccine to help prevent it,” Dr. Yang stated in a news release. “Our study results may encourage people ages 50 and older to follow the recommendation and get vaccinated against shingles. You are reducing the risk of shingles, and at the same time, you may be reducing your risk of stroke.”

“Further studies are needed to confirm our findings of association between Zostavax vaccine and risk of stroke,” Dr. Yang said.

Because the CDC Advisory Committee on Immunization Practices recommended Shingrix vaccine only for healthy adults 50 years and older in 2017, there were insufficient data in Medicare to study the association between that vaccine and risk of stroke at the time of the current study.

“However, two doses of Shingrix are more than 90% effective at preventing shingles and postherpetic neuralgia, and higher than that of Zostavax,” Dr. Yang said.

‘Very intriguing’ research

“This is a very interesting study,” Ralph L. Sacco, MD, past president of the American Heart Association, said in a video commentary released in advance of the conference. It was a very large sample, he noted, and those older than age 60 years who had the vaccine were protected with a lower risk for both ischemic and hemorrhagic stroke.

“So it is very intriguing,” added Dr. Sacco, chairman of the department of neurology at the University of Miami. “We know things like shingles can increase inflammation and increase the risk of stroke,” Dr. Sacco said, “but this is the first time in a very large Medicare database that it was shown that those who had the vaccine had a lower risk of stroke.”

The CDC funded this study. Dr. Yang and Dr. Sacco have disclosed no relevant financial relationships.

SOURCE: Yang Q et al. ISC 2020, Abstract TP493.

This article first appeared on Medscape.com.

LOS ANGELES – Prevention of shingles with the Zoster Vaccine Live may reduce the risk of subsequent stroke among older adults as well, the first study to examine this association suggests. Shingles vaccination was linked to a 20% decrease in stroke risk in people younger than 80 years of age in the large Medicare cohort study. Older participants showed a 10% reduced risk, according to data released in advance of formal presentation at this week’s International Stroke Conference, sponsored by the American Heart Association.

Reductions were seen for both ischemic and hemorrhagic events.

“Our findings might encourage people age 50 or older to get vaccinated against shingles and to prevent shingles-associated stroke risk,” Quanhe Yang, PhD, lead study author and senior scientist at the Centers for Disease Control and Prevention, said in an interview.

Dr. Yang and colleagues evaluated the only shingles vaccine available at the time of the study, Zoster Vaccine Live (Zostavax). However, the CDC now calls an adjuvanted, nonlive recombinant vaccine (Shingrix) the preferred shingles vaccine for healthy adults aged 50 years and older. Shingrix was approved in 2017. Zostavax, approved in 2006, can still be used in healthy adults aged 60 years and older, the agency states.

A reduction in inflammation from Zoster Vaccine Live may be the mechanism by which stroke risk is reduced, Dr. Yang said. The newer vaccine, which the CDC notes is more than 90% effective, might provide even greater protection against stroke, although more research is needed, he added.

Interestingly, prior research suggested that, once a person develops shingles, it may be too late. Dr. Yang and colleagues showed vaccination or antiviral treatment after a shingles episode was not effective at reducing stroke risk in research presented at the 2019 International Stroke Conference.

Shingles can present as a painful reactivation of chickenpox, also known as the varicella-zoster virus. Shingles is also common; Dr. Yang estimated one in three people who had chickenpox will develop the condition at some point in their lifetime. In addition, researchers have linked shingles to an elevated risk of stroke.

To assess the vaccine’s protective effect on stroke, Dr. Yang and colleagues reviewed health records for 1.38 million Medicare recipients. All participants were aged 66 years or older, had no history of stroke at baseline, and received the Zoster Vaccine Live during 2008-2016. The investigators compared the stroke rate in this vaccinated group with the rate in a matched control group of the same number of Medicare fee-for-service beneficiaries who did not receive the vaccination. They adjusted their analysis for age, sex, race, medications, and comorbidities.

The overall decrease of 16% in stroke risk associated with vaccination included a 12% drop in hemorrhagic stroke and 18% decrease in ischemic stroke over a median follow-up of 3.9 years follow-up (interquartile range, 2.7-5.4).

The adjusted hazard ratios comparing the vaccinated with control groups were 0.84 (95% confidence interval, 0.83-0.85) for all stroke; 0.82 (95% CI, 0.81-0.83) for acute ischemic stroke; and 0.88 (95% CI, 0.84-0.91) for hemorrhagic stroke.

The vaccinated group experienced 42,267 stroke events during that time. This rate included 33,510 acute ischemic strokes and 4,318 hemorrhagic strokes. At the same time, 48,139 strokes occurred in the control group. The breakdown included 39,334 ischemic and 4,713 hemorrhagic events.

“Approximately 1 million people in the United States get shingles each year, yet there is a vaccine to help prevent it,” Dr. Yang stated in a news release. “Our study results may encourage people ages 50 and older to follow the recommendation and get vaccinated against shingles. You are reducing the risk of shingles, and at the same time, you may be reducing your risk of stroke.”

“Further studies are needed to confirm our findings of association between Zostavax vaccine and risk of stroke,” Dr. Yang said.

Because the CDC Advisory Committee on Immunization Practices recommended Shingrix vaccine only for healthy adults 50 years and older in 2017, there were insufficient data in Medicare to study the association between that vaccine and risk of stroke at the time of the current study.

“However, two doses of Shingrix are more than 90% effective at preventing shingles and postherpetic neuralgia, and higher than that of Zostavax,” Dr. Yang said.

‘Very intriguing’ research

“This is a very interesting study,” Ralph L. Sacco, MD, past president of the American Heart Association, said in a video commentary released in advance of the conference. It was a very large sample, he noted, and those older than age 60 years who had the vaccine were protected with a lower risk for both ischemic and hemorrhagic stroke.

“So it is very intriguing,” added Dr. Sacco, chairman of the department of neurology at the University of Miami. “We know things like shingles can increase inflammation and increase the risk of stroke,” Dr. Sacco said, “but this is the first time in a very large Medicare database that it was shown that those who had the vaccine had a lower risk of stroke.”

The CDC funded this study. Dr. Yang and Dr. Sacco have disclosed no relevant financial relationships.

SOURCE: Yang Q et al. ISC 2020, Abstract TP493.

This article first appeared on Medscape.com.

COVID-19, the infection caused by the newly identified coronavirus, is a currently a disease with no pharmaceutical weapons against it. There’s no vaccine to prevent it, and no drugs can treat it.

But researchers are racing to change that. A vaccine could be ready to test as soon as April. More than two dozen studies have already been registered on ClinicalTrials.gov, a website that tracks research. These studies aim to test everything from traditional Chinese medicine to vitamin C, stem cells, steroids, and medications that fight other viruses, like the flu and HIV. The hope is that something about how these repurposed remedies work will help patients who are desperately ill with no other prospects.

Anthony Fauci, MD, director of the National Institute of Allergy and Infectious Diseases, says this is all part of the playbook for brand-new diseases. “There’s a lot of empiric guessing,” he says. “They’re going to propose a whole lot of drugs that already exist. They’re going to say, here’s the data that shows it blocks the virus” in a test tube. But test tubes aren’t people, and many drugs that seem to work in a lab won’t end up helping patients.

Coronaviruses are especially hard to stop once they invade the body. Unlike many other kinds of viruses, they have a fail-safe against tampering – a “proofreader” that constantly inspects their code, looking for errors, including the potentially life-saving errors that drugs could introduce.

Dr. Fauci said that researchers will be able to make better guesses about how to help people when they can try drugs in animals. “We don’t have an animal model yet of the new coronavirus. When we do get an animal model, that will be a big boon to drugs because then, you can clearly test them in a physiological way, whether they work,” he says.

Looking to drugs for HIV and flu

One of the drugs already under study is the combination of two HIV medications: lopinavir and ritonavir (Kaletra). Kaletra stops viruses by interfering with the enzymes they need to infect cells, called proteases.

One study being done at the Guangzhou Eighth People’s Hospital in China is testing Kaletra against Arbidol, an antiviral drug approved in China and Russia to treat the flu. Two groups of patients will take the medications along with standard care. A third group in the study will receive only standard care, typically supportive therapy with oxygen and IV fluids that are meant to support the body so the immune system can fight off a virus on its own.

An Ebola drug gets a second look

One repurposed drug generating a lot of buzz is an experimental infusion called remdesivir (Xembify). It was originally tested against the Ebola virus. While it didn’t work for that infection, it has been shown to shut down the new coronavirus, at least in test tubes. It’s been given to a small number of COVID-19 patients already, including one in Washington state.

In order to have better evidence of how well it may work in people, two studies in Beijing are comparing remdesivir to a dummy pill to see if the drug can help patients with both mild and severe symptoms recover from their illnesses. Viruses work by infecting cells, taking over their machinery, and getting them to crank out more copies of the virus, which then goes on to infect more cells. Remdesivir is a mimic that fools a virus into replacing one of its four building blocks with a chemical fake. Once in the virus’s blueprints, the imposter acts like a stop sign that keeps the virus from copying itself.

Other kinds of drugs in the same class – called nucleotide analogs – are used to attack cancer and other infectious viruses like hepatitis.

Last week, Chinese scientists published study showing remdesivir was effective against the new coronavirus, 2019-nCoV. Out of seven drugs tested, only remdesivir and an older drug called chloroquine (Aralen), which is used to treat malaria, worked, at least in test tubes. “It functions like a knife that just cuts off the RNA strand,” says Mark Denison, MD, a pediatric infectious disease specialist at Vanderbilt University in Nashville. “They can’t replicate any more. It stops them from doing that.” Dr. Denison is part of a team of researchers in Tennessee and North Carolina that discovered remdesivir could stop coronaviruses, like severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS), in test tubes and animals. He has studied coronaviruses in his lab for 30 years. He knew they would pose a threat again. “We’re shocked, but not surprised, that this has happened again,” he says of the China-based outbreak of 2019-nCoV.

After the SARS outbreak, which infected more than 8,000 people in 26 countries during 2002-2003, and MERS, which has infected nearly 2,500 people in 27 countries since 2012, researchers knew they had to start looking for treatments that would work against coronaviruses. Dr. Denison reached out to Gilead Sciences, a company best known for its antiviral medications that treat HIV and hepatitis C, and asked it to send drug candidates for him to test on coronaviruses. “The idea was that we didn’t want a drug that would just work against SARS or MERS,” he says. “We wanted drugs that worked against every coronavirus.”

Many of the agents he tried didn’t work until Dr. Denison and his team knocked out the virus’s pesky proofreader. Remdesivir seems to be able to defeat the proofreader, though Dr. Denison admits that he does not know how the drug gets around a virus’s defenses. He has a grant from the National Institutes of Health to study that. Gilead has been giving remdesivir to “a small number” of coronavirus patients in the United States and Europe on a compassionate basis.

One of those patients was a 35-year-old man in Everett, Wash., who had gotten pneumonia after being infected with the new coronavirus during a trip to see family in Wuhan, China, the epicenter of the outbreak. His doctors started IV remdesivir on the evening of his 7th day in the hospital. On the 8th day, he improved. He was well enough to stop using oxygen. Signs of pneumonia were gone. He got his appetite back. His case was recently published in the New England Journal of Medicine, igniting a firestorm of interest in the therapy.

Unfortunately, though, even Dr. Denison says a single person’s case isn’t enough proof that the medication can treat the new coronavirus. The patient, who has not been identified, was getting expert care. He may have improved on his own, despite getting the drug. He said the challenge in people will be to find out two things: whether the medication can block the spread of virus in the body and whether it can reverse the disease. “You can remove the source of injury, but you still have the injury,” he said. Other important questions include how soon the drug may need to be given after infection for it work and whether it may cause significant side effects.

A promising pill

Another drug, a nucleoside analog, that appears to be able to defeat the coronavirus proofreader, EIDD-2801, was developed by Emory University in Atlanta. It was originally intended to treat the flu but has shown some effectiveness against coronaviruses like SARS and MERS.

The FDA recently reached out to Emory asking if it had any drug candidates that might work against the new coronavirus. “It’s a good shot on goal here,” says George Painter, PhD, CEO of Drug Innovation Ventures at Emory. EIDD-2801 can be taken as a pill, which makes it easier to use outside of a hospital setting.

“The capsules for the trial are being made at the end of this month. So we’re close,” Painter says. “We’re right on the edge.”

While these early tests are just getting started, and it will be months until researchers have results, the World Health Organization has sounded a note of caution.

In new guidelines for the clinical management of COVID-19, the WHO reminded doctors and patients that there’s not enough evidence to recommend any specific treatment for infected patients.

Right now, the guidelines recommend that doctors offer supportive care to help the body fight off an infection on its own.

The organization says unlicensed treatments should be given only in the context of clinical trials that have been ethically reviewed or with strict clinical monitoring in emergencies.
 

This article first appeared on WebMD.com.

COVID-19, the infection caused by the newly identified coronavirus, is a currently a disease with no pharmaceutical weapons against it. There’s no vaccine to prevent it, and no drugs can treat it.

But researchers are racing to change that. A vaccine could be ready to test as soon as April. More than two dozen studies have already been registered on ClinicalTrials.gov, a website that tracks research. These studies aim to test everything from traditional Chinese medicine to vitamin C, stem cells, steroids, and medications that fight other viruses, like the flu and HIV. The hope is that something about how these repurposed remedies work will help patients who are desperately ill with no other prospects.

Anthony Fauci, MD, director of the National Institute of Allergy and Infectious Diseases, says this is all part of the playbook for brand-new diseases. “There’s a lot of empiric guessing,” he says. “They’re going to propose a whole lot of drugs that already exist. They’re going to say, here’s the data that shows it blocks the virus” in a test tube. But test tubes aren’t people, and many drugs that seem to work in a lab won’t end up helping patients.

Coronaviruses are especially hard to stop once they invade the body. Unlike many other kinds of viruses, they have a fail-safe against tampering – a “proofreader” that constantly inspects their code, looking for errors, including the potentially life-saving errors that drugs could introduce.

Dr. Fauci said that researchers will be able to make better guesses about how to help people when they can try drugs in animals. “We don’t have an animal model yet of the new coronavirus. When we do get an animal model, that will be a big boon to drugs because then, you can clearly test them in a physiological way, whether they work,” he says.

Looking to drugs for HIV and flu

One of the drugs already under study is the combination of two HIV medications: lopinavir and ritonavir (Kaletra). Kaletra stops viruses by interfering with the enzymes they need to infect cells, called proteases.

One study being done at the Guangzhou Eighth People’s Hospital in China is testing Kaletra against Arbidol, an antiviral drug approved in China and Russia to treat the flu. Two groups of patients will take the medications along with standard care. A third group in the study will receive only standard care, typically supportive therapy with oxygen and IV fluids that are meant to support the body so the immune system can fight off a virus on its own.

An Ebola drug gets a second look

One repurposed drug generating a lot of buzz is an experimental infusion called remdesivir (Xembify). It was originally tested against the Ebola virus. While it didn’t work for that infection, it has been shown to shut down the new coronavirus, at least in test tubes. It’s been given to a small number of COVID-19 patients already, including one in Washington state.

In order to have better evidence of how well it may work in people, two studies in Beijing are comparing remdesivir to a dummy pill to see if the drug can help patients with both mild and severe symptoms recover from their illnesses. Viruses work by infecting cells, taking over their machinery, and getting them to crank out more copies of the virus, which then goes on to infect more cells. Remdesivir is a mimic that fools a virus into replacing one of its four building blocks with a chemical fake. Once in the virus’s blueprints, the imposter acts like a stop sign that keeps the virus from copying itself.

Other kinds of drugs in the same class – called nucleotide analogs – are used to attack cancer and other infectious viruses like hepatitis.

Last week, Chinese scientists published study showing remdesivir was effective against the new coronavirus, 2019-nCoV. Out of seven drugs tested, only remdesivir and an older drug called chloroquine (Aralen), which is used to treat malaria, worked, at least in test tubes. “It functions like a knife that just cuts off the RNA strand,” says Mark Denison, MD, a pediatric infectious disease specialist at Vanderbilt University in Nashville. “They can’t replicate any more. It stops them from doing that.” Dr. Denison is part of a team of researchers in Tennessee and North Carolina that discovered remdesivir could stop coronaviruses, like severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS), in test tubes and animals. He has studied coronaviruses in his lab for 30 years. He knew they would pose a threat again. “We’re shocked, but not surprised, that this has happened again,” he says of the China-based outbreak of 2019-nCoV.

After the SARS outbreak, which infected more than 8,000 people in 26 countries during 2002-2003, and MERS, which has infected nearly 2,500 people in 27 countries since 2012, researchers knew they had to start looking for treatments that would work against coronaviruses. Dr. Denison reached out to Gilead Sciences, a company best known for its antiviral medications that treat HIV and hepatitis C, and asked it to send drug candidates for him to test on coronaviruses. “The idea was that we didn’t want a drug that would just work against SARS or MERS,” he says. “We wanted drugs that worked against every coronavirus.”

Many of the agents he tried didn’t work until Dr. Denison and his team knocked out the virus’s pesky proofreader. Remdesivir seems to be able to defeat the proofreader, though Dr. Denison admits that he does not know how the drug gets around a virus’s defenses. He has a grant from the National Institutes of Health to study that. Gilead has been giving remdesivir to “a small number” of coronavirus patients in the United States and Europe on a compassionate basis.

One of those patients was a 35-year-old man in Everett, Wash., who had gotten pneumonia after being infected with the new coronavirus during a trip to see family in Wuhan, China, the epicenter of the outbreak. His doctors started IV remdesivir on the evening of his 7th day in the hospital. On the 8th day, he improved. He was well enough to stop using oxygen. Signs of pneumonia were gone. He got his appetite back. His case was recently published in the New England Journal of Medicine, igniting a firestorm of interest in the therapy.

Unfortunately, though, even Dr. Denison says a single person’s case isn’t enough proof that the medication can treat the new coronavirus. The patient, who has not been identified, was getting expert care. He may have improved on his own, despite getting the drug. He said the challenge in people will be to find out two things: whether the medication can block the spread of virus in the body and whether it can reverse the disease. “You can remove the source of injury, but you still have the injury,” he said. Other important questions include how soon the drug may need to be given after infection for it work and whether it may cause significant side effects.

A promising pill

Another drug, a nucleoside analog, that appears to be able to defeat the coronavirus proofreader, EIDD-2801, was developed by Emory University in Atlanta. It was originally intended to treat the flu but has shown some effectiveness against coronaviruses like SARS and MERS.

The FDA recently reached out to Emory asking if it had any drug candidates that might work against the new coronavirus. “It’s a good shot on goal here,” says George Painter, PhD, CEO of Drug Innovation Ventures at Emory. EIDD-2801 can be taken as a pill, which makes it easier to use outside of a hospital setting.

“The capsules for the trial are being made at the end of this month. So we’re close,” Painter says. “We’re right on the edge.”

While these early tests are just getting started, and it will be months until researchers have results, the World Health Organization has sounded a note of caution.

In new guidelines for the clinical management of COVID-19, the WHO reminded doctors and patients that there’s not enough evidence to recommend any specific treatment for infected patients.

Right now, the guidelines recommend that doctors offer supportive care to help the body fight off an infection on its own.

The organization says unlicensed treatments should be given only in the context of clinical trials that have been ethically reviewed or with strict clinical monitoring in emergencies.
 

This article first appeared on WebMD.com.

COVID-19, the infection caused by the newly identified coronavirus, is a currently a disease with no pharmaceutical weapons against it. There’s no vaccine to prevent it, and no drugs can treat it.

But researchers are racing to change that. A vaccine could be ready to test as soon as April. More than two dozen studies have already been registered on ClinicalTrials.gov, a website that tracks research. These studies aim to test everything from traditional Chinese medicine to vitamin C, stem cells, steroids, and medications that fight other viruses, like the flu and HIV. The hope is that something about how these repurposed remedies work will help patients who are desperately ill with no other prospects.

Anthony Fauci, MD, director of the National Institute of Allergy and Infectious Diseases, says this is all part of the playbook for brand-new diseases. “There’s a lot of empiric guessing,” he says. “They’re going to propose a whole lot of drugs that already exist. They’re going to say, here’s the data that shows it blocks the virus” in a test tube. But test tubes aren’t people, and many drugs that seem to work in a lab won’t end up helping patients.

Coronaviruses are especially hard to stop once they invade the body. Unlike many other kinds of viruses, they have a fail-safe against tampering – a “proofreader” that constantly inspects their code, looking for errors, including the potentially life-saving errors that drugs could introduce.

Dr. Fauci said that researchers will be able to make better guesses about how to help people when they can try drugs in animals. “We don’t have an animal model yet of the new coronavirus. When we do get an animal model, that will be a big boon to drugs because then, you can clearly test them in a physiological way, whether they work,” he says.

Looking to drugs for HIV and flu

One of the drugs already under study is the combination of two HIV medications: lopinavir and ritonavir (Kaletra). Kaletra stops viruses by interfering with the enzymes they need to infect cells, called proteases.

One study being done at the Guangzhou Eighth People’s Hospital in China is testing Kaletra against Arbidol, an antiviral drug approved in China and Russia to treat the flu. Two groups of patients will take the medications along with standard care. A third group in the study will receive only standard care, typically supportive therapy with oxygen and IV fluids that are meant to support the body so the immune system can fight off a virus on its own.

An Ebola drug gets a second look

One repurposed drug generating a lot of buzz is an experimental infusion called remdesivir (Xembify). It was originally tested against the Ebola virus. While it didn’t work for that infection, it has been shown to shut down the new coronavirus, at least in test tubes. It’s been given to a small number of COVID-19 patients already, including one in Washington state.

In order to have better evidence of how well it may work in people, two studies in Beijing are comparing remdesivir to a dummy pill to see if the drug can help patients with both mild and severe symptoms recover from their illnesses. Viruses work by infecting cells, taking over their machinery, and getting them to crank out more copies of the virus, which then goes on to infect more cells. Remdesivir is a mimic that fools a virus into replacing one of its four building blocks with a chemical fake. Once in the virus’s blueprints, the imposter acts like a stop sign that keeps the virus from copying itself.

Other kinds of drugs in the same class – called nucleotide analogs – are used to attack cancer and other infectious viruses like hepatitis.

Last week, Chinese scientists published study showing remdesivir was effective against the new coronavirus, 2019-nCoV. Out of seven drugs tested, only remdesivir and an older drug called chloroquine (Aralen), which is used to treat malaria, worked, at least in test tubes. “It functions like a knife that just cuts off the RNA strand,” says Mark Denison, MD, a pediatric infectious disease specialist at Vanderbilt University in Nashville. “They can’t replicate any more. It stops them from doing that.” Dr. Denison is part of a team of researchers in Tennessee and North Carolina that discovered remdesivir could stop coronaviruses, like severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS), in test tubes and animals. He has studied coronaviruses in his lab for 30 years. He knew they would pose a threat again. “We’re shocked, but not surprised, that this has happened again,” he says of the China-based outbreak of 2019-nCoV.

After the SARS outbreak, which infected more than 8,000 people in 26 countries during 2002-2003, and MERS, which has infected nearly 2,500 people in 27 countries since 2012, researchers knew they had to start looking for treatments that would work against coronaviruses. Dr. Denison reached out to Gilead Sciences, a company best known for its antiviral medications that treat HIV and hepatitis C, and asked it to send drug candidates for him to test on coronaviruses. “The idea was that we didn’t want a drug that would just work against SARS or MERS,” he says. “We wanted drugs that worked against every coronavirus.”

Many of the agents he tried didn’t work until Dr. Denison and his team knocked out the virus’s pesky proofreader. Remdesivir seems to be able to defeat the proofreader, though Dr. Denison admits that he does not know how the drug gets around a virus’s defenses. He has a grant from the National Institutes of Health to study that. Gilead has been giving remdesivir to “a small number” of coronavirus patients in the United States and Europe on a compassionate basis.

One of those patients was a 35-year-old man in Everett, Wash., who had gotten pneumonia after being infected with the new coronavirus during a trip to see family in Wuhan, China, the epicenter of the outbreak. His doctors started IV remdesivir on the evening of his 7th day in the hospital. On the 8th day, he improved. He was well enough to stop using oxygen. Signs of pneumonia were gone. He got his appetite back. His case was recently published in the New England Journal of Medicine, igniting a firestorm of interest in the therapy.

Unfortunately, though, even Dr. Denison says a single person’s case isn’t enough proof that the medication can treat the new coronavirus. The patient, who has not been identified, was getting expert care. He may have improved on his own, despite getting the drug. He said the challenge in people will be to find out two things: whether the medication can block the spread of virus in the body and whether it can reverse the disease. “You can remove the source of injury, but you still have the injury,” he said. Other important questions include how soon the drug may need to be given after infection for it work and whether it may cause significant side effects.

A promising pill

Another drug, a nucleoside analog, that appears to be able to defeat the coronavirus proofreader, EIDD-2801, was developed by Emory University in Atlanta. It was originally intended to treat the flu but has shown some effectiveness against coronaviruses like SARS and MERS.

The FDA recently reached out to Emory asking if it had any drug candidates that might work against the new coronavirus. “It’s a good shot on goal here,” says George Painter, PhD, CEO of Drug Innovation Ventures at Emory. EIDD-2801 can be taken as a pill, which makes it easier to use outside of a hospital setting.

“The capsules for the trial are being made at the end of this month. So we’re close,” Painter says. “We’re right on the edge.”

While these early tests are just getting started, and it will be months until researchers have results, the World Health Organization has sounded a note of caution.

In new guidelines for the clinical management of COVID-19, the WHO reminded doctors and patients that there’s not enough evidence to recommend any specific treatment for infected patients.

Right now, the guidelines recommend that doctors offer supportive care to help the body fight off an infection on its own.

The organization says unlicensed treatments should be given only in the context of clinical trials that have been ethically reviewed or with strict clinical monitoring in emergencies.
 

This article first appeared on WebMD.com.