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COVID-19 Updates – Recap of Videos 57-60

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    Here’s a summary of this week’s latest updates on the global COVID-19 pandemic. Check out these videos and all of our other lectures at MedCram.com or on our YouTube page

     

    Remdesivir Treatment Update and Can Far-UVC Disinfect Public Spaces?

    In our 57th video update on the novel coronavirus pandemic, Dr. Seheult shares the link to the updated Johns Hopkins dashboard, including maps of the world and the United States, fatality rates, critical trends, and more. He shares updates on the drug Remdesivir, which we first introduced in video 11 and explained in greater detail in video 33. A report published in STAT shared that early peeks at the data show promise for Remdesivir, to treat patients with COVID-19… but this data and source may not be substantiated.

    In other news, Dr. Seheult looks at the potential of ultraviolet light, specifically far-UVC, to control the spread of aerosolized viral particles, such as influenza or COVID-19, without damaging human skin. Thus, the use of far-UVC light in public spaces could play a significant role in lifting shelter-in-place mandates and other shutdowns. The biggest roadblocks, however, are pending FDA approval and availability (and cost) of far-UVC lamps and products. 

     

    Testing; Causes of Hypoxemia in COVID-19 (V/Q vs Shunt vs Diffusion)

    In our 58th COVID-19 update, Dr. Seheult looks at two reports of antibody testing, one in Chelsea, Massachusetts and the other in Santa Clara County, California. Both of these reports suggest much more widespread infection rates than currently reported. However, Dr. Seheult discusses the limitations of each report and testing method, as well as the importance of peer reviews, such as this one that looked at the Santa Clara County report.

    Switching gears, Dr. Seheult discusses the three types of hypoxemia — V/Q mismatch, shunting, and diffusion abnormalities — and their mechanisms in COVID-19. For an even deeper look at hypoxemia, check out our free Hypoxemia Explained Clearly course at MedCram.com. 

     

    Coronavirus Pandemic Update 59: Dr. Seheult’s Daily Regimen (Vitamin D, C, Zinc, Quercetin, NAC)

    Our 59th coronavirus pandemic update brings practical advice for staying healthy from Dr. Seheult’s daily regimen, again highlighting the importance of sleep. He talks about supplementing with vitamins C and D, as well as quercetin, a zinc ionophore that can also be found in onions, capers, and other food products. Dr. Seheult also talks about supplementing with zinc and NAC, or N-acetylcysteine, which has been shown to significantly attenuate severity of the influenza virus

    For staying safe at work, Dr. Seheult also details his daily process starting with supplies to keep in your car, entering and exiting the hospital, strategies for dressing and undressing, and even his showering methods (and hydrothermal therapy) once arriving back at home. 

     

    Hydroxychloroquine Update; NYC Data; How Widespread is COVID-19?

    In our 60th COVID-19 video update, Dr. Seheult reviews numbers across the globe, as well as a new study looking at blood samples of residents of Los Angeles county, which predicted that the actual infection rate may be up to 40 times greater than previously reported. Dr. Seheult also addresses why men might be more likely to contract COVID-19, referencing this GQ article, in which Dr. Seheult comments on differences in innate immunity for men and women.  

    In addition, Dr. Seheult looks at the latest study on hydroxychloroquine, citing this article in GoodRx, which overviews several studies on its effectiveness in treating COVID-19. He also cites articles on utilizing prone position for patients with ARDS or while on the ventilator, as well as this article summarizing the characteristics, comorbidities, and outcomes of COVID-19 patients in the New York City area.

     

    More Updates and Information to Come!

    We’ve got more COVID-19 updates and resources in the works, so stay tuned to MedCram.com and our YouTube channel for the latest information. 

    Meanwhile, here’s a list of all the resources we’ve shared so far:

    1. Coronavirus Outbreak, Transmission, and Pathophysiology
    2. Coronavirus Symptoms, Diagnosis, and Treatment
    3. Coronavirus Update 3: Spread, Quarantine, Projections, and Vaccine
    4. How Coronavirus Kills: Acute Respiratory Distress Syndrome (ARDS) & Treatment
    5. Coronavirus Epidemic Update 5: Mortality Rate vs SARS / Influenza
    6. Coronavirus Outbreak Update 6: Asymptomatic Transmission & Incubation Period
    7. Coronavirus Epidemic Update 7: Global Health Emergency Declared, Viral Shedding
    8. Coronavirus Outbreak Update 8: Travel Ban, Spread Outside of China, Quarantine, & MRSA
    9. Coronavirus Epidemic Update 9: Fecal-Oral Transmission, Recovery vs Death Rate
    10. Coronavirus Epidemic Update 10: New Studies, Transmission, Spread from Wuhan, Prevention (nocv 2019)
    11. Coronavirus Epidemic Update 11: Antiviral Drugs, Treatment Trials for nCoV (Remdesivir, Chloroquine)
    12. Coronavirus Epidemic Update 12: Unsupported Theories, Pneumonia, ACE2 & nCoV
    13. Garage Talk Podcast — Dr. Roger Seheult and the Coronavirus
    14. Coronavirus Epidemic Update 13: Li Wenliang, nCoV vs Influenza, Dip in Daily Cases, Spread to Canada
    15. Forbes Article – Medical Experts Employ Social Media To Battle Coronavirus
    16. Coronavirus Epidemic Update 14: Hospital spread of infection, WHO allowed in China, N-95 masks
    17. Coronavirus Epidemic Update 15: Underreporting, Prevention, 24 Day Incubation? (COVID19)
    18. Coronavirus Epidemic Update 16: Strengthening Your Immune Response to Viral Infections (COVID-19)
    19. Coronavirus Epidemic Update 17: Spike in Confirmed Cases, Fighting Infections with Sleep (COVID-19)
    20. Coronavirus Epidemic Update 18: Cellphone Tracking, Increase in Hospitalizations, More Sleep Tips
    21. Coronavirus Epidemic Update 19: Treatment and Medication Clinical Trials
    22. Coronavirus Epidemic Update 20: Misinformation Spread, Infection Severity, Cruise Ship, Origins
    23. Coronavirus Epidemic Update 21: Antibodies, Case Fatality, Clinical Recommendations, 2nd Infections?
    24. Coronavirus Epidemic Update 22: Spread Without Symptoms, Cruise Quarantine, Asymptomatic Testing
    25. Coronavirus Epidemic Update 23: Infections in Kids & Pregnancy, South Korea, Spillover From Bats
    26. Coronavirus Epidemic Update 24: Infections in Italy, Transmissibility, COVID-19 Symptoms
    27. Coronavirus Epidemic Update 25: Vaccine Developments, Italy’s Response, and Mortality Rate Trends
    28. How Viruses Work – Molecular Biology Simplified (DNA, RNA, Protein Synthesis)
    29. Coronavirus Epidemic Update 26: Treatment Updates, Stock Markets, Germany & San Francisco, Pandemic?
    30. Coronavirus Epidemic Update 27: Testing accuracy for COVID-19 (CT Scan vs. RT-PCR), California Cases
    31. Coronavirus Epidemic Update 28: Practical Prevention Strategies, Patient Age vs. Case Fatality Rate
    32. Coronavirus Epidemic Update 29: Testing problems, mutations, COVID-19 in Washington & Iran
    33. Coronavirus Epidemic Update 30: More Global COVID-19 Outbreaks, Vitamin D May Aid Prevention
    34. Coronavirus Epidemic Update 31: Mortality Rate, Cleaning Products, A More/Less Severe Virus Strain?
    35. Coronavirus Epidemic Update 32: Important Data from South Korea, Can Zinc Help Prevent COVID-19?
    36. Coronavirus Epidemic Update 33: COVID-19 Medication Treatment Trials, Global Testing Remains Limited
    37. Coronavirus Epidemic Update 34: US Cases Surge, Chloroquine & Zinc Treatment Combo, Italy Lockdown
    38. Coronavirus Pandemic Update 35: New Outbreaks & Travel Restrictions, Possible COVID-19 Treatments
    39. Coronavirus Pandemic Update 36: Flatten The COVID-19 Curve, Social Distancing, Hospital Capacities
    40. Coronavirus Pandemic Update 37: The ACE-2 Receptor – The Doorway to COVID-19 (ACE Inhibitors & ARBs)
    41. Coronavirus Pandemic Update 38: How Hospitals & Clinics Can Prepare for COVID-19, Global Cases Surge
    42. Coronavirus Pandemic Update 39: Rapid COVID-19 Spread with Mild or No Symptoms, More on Treatment
    43. Coronavirus Pandemic Update 40: Ibuprofen and COVID-19 (are NSAIDs safe?), Trials of HIV medications
    44. Coronavirus Pandemic Update 41: Shelter In Place, FDA Investigates Hydroxychloroquine for COVID-19
    45. COVID-19 Ventilator Course: Learn or Review Mechanical Ventilation (Free at MedCram.com)
    46. Coronavirus Pandemic Update 42: Immunity to COVID-19 and is Reinfection Possible?
    47. Coronavirus Pandemic Update 43: Shortages, Immunity, & Can a TB Vaccine (BCG) Help Prevent COVID-19?
    48. Coronavirus Pandemic Update 44: Loss of Smell & Conjunctivitis in COVID-19, Is Fever Helpful?
    49. Coronavirus Pandemic Update 45: Sharing Ventilators, More on Sleep, Immunity, & COVID-19 Prevention
    50. Coronavirus Pandemic Update 46: Can Hot/Cold Therapy Boost Immunity? More on Hydroxychloroquine
    51. Coronavirus Pandemic Update 47: Searching for Immunity Boosters & Possible Lessons From Spanish Flu
    52. Coronavirus Pandemic Update 48: Curve Flattening in California, PPE in the ICU, Medication Trials
    53. Coronavirus Pandemic Update 49: New Data on COVID-19 vs Other Viral Infections (Ventilator Outcomes)
    54. Coronavirus Pandemic Update 50: Dip in Daily New Deaths; Research on Natural Killer Cells & COVID-19
    55. Coronavirus Pandemic Update 51: State by State Projections; Ultrasound to Diagnose COVID19 Pneumonia
    56. Lung Ultrasound in COVID 19: Findings, Accuracy, Pneumonia Diagnosis, Utility (POCUS)
    57. Coronavirus Pandemic Update 52: Ivermectin Treatment; Does COVID-19 Attack Hemoglobin?
    58. Coronavirus Pandemic Update 53: Anticoagulation; Can Mechanical Ventilation Make COVID 19 Worse?
    59. Coronavirus Pandemic Update 54: COVID-19 Antibody vs. PCR Testing; When to Relax Social Distancing?
    60. Coronavirus Pandemic Update 55: How COVID-19 Infection Attacks The Immune System & Differs From HIV
    61. Coronavirus Pandemic Update 56: What is “Forest Bathing” & Can It Boost Immunity Against Viruses?
    62. Coronavirus Pandemic Update 57: Remdesivir Treatment Update and Can Far-UVC Disinfect Public Spaces?
    63. Coronavirus Pandemic Update 58: Testing; Causes of Hypoxemia in COVID-19 (V/Q vs Shunt vs Diffusion)
    64. Coronavirus Pandemic Update 59: Dr. Seheult’s Daily Regimen (Vitamin D, C, Zinc, Quercetin, NAC)
    65. Coronavirus Pandemic Update 60: Hydroxychloroquine Update; NYC Data; How Widespread is COVID-19?

     

    5 Comments

    1. Bunny Reveglia on May 1, 2020 at 11:27 pm

      For treating the oxidative stress in Covid-19 patients has anyone tried this Chinese herb for endothelial nitric oxide production? It can be taken in tea form. Here is the scientific article
      https://pubmed.ncbi.nlm.nih.gov/7804367/

    2. Daif on May 5, 2020 at 4:27 pm

      I have researched in the same direction and found that there are good evidence that Ursolic Acid can help inhibit superoxide. It is an OTC supplement well known to the fitness community.
      https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4216084/ among other references.
      Coupled with vitamin A C E, Melatonin and NAC may prove beneficial for preserving endothelial integrity. If we add to that Zinc, QUERCETIN and vitamin D. (And in some cases a baby Aspirin (100 mg) for it’s antiplatlet activity
      Based on different findings so far, would one consider the above as good prophylactic stack? Of course, one should be attentive to any contradictions!!!
      *PS: I would like to forward some material on the subject to DR Seheult. Can anyone advise/instruct how I can contact him?
      Thanks and do keep safe!

      • Brian Smith on July 19, 2020 at 8:30 pm

        I understand the virus’s prescence is being verified by the bodies response but no one has yet isolated the virus in its sterile form (separate from human tissue fluids etc) to actually identify this virus. It’s being measured I here by the bodies immune response or response to damage from a virus but no one has actually done the necessary lab experiments,anywhere in the world, of isolating a sterile virus to identify.
        How can a vaccine be created for something that has not been verified.

    3. John Tooker on May 21, 2020 at 5:31 pm

      STAT
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      IN THE LAB
      ‘It’s something I have never seen’: How the Covid-19 virus hijacks cells
      By SHARON BEGLEY @sxbegle

      MAY 21, 2020

      RNA (green)
      RNA (in green) from the SARS-CoV-2 virus is shown taking over the cells it infects.
      ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI
      Adeep dive into how the new coronavirus infects cells has found that it orchestrates a hostile takeover of their genes unlike any other known viruses do, producing what one leading scientist calls “unique” and “aberrant” changes.

      Recent studies show that in seizing control of genes in the human cells it invades, the virus changes how segments of DNA are read, doing so in a way that might explain why the elderly are more likely to die of Covid-19 and why antiviral drugs might not only save sick patients’ lives but also prevent severe disease if taken before infection.

      “It’s something I have never seen in my 20 years of” studying viruses, said virologist Benjamin tenOever of the Icahn School of Medicine at Mount Sinai, referring to how SARS-CoV-2, the virus that causes Covid-19, hijacks cells’ genomes.

      The “something” he and his colleagues saw is how SARS-CoV-2 blocks one virus-fighting set of genes but allows another set to launch, a pattern never seen with other viruses. Influenza and the original SARS virus (in the early 2000s), for instance, interfere with both arms of the body’s immune response — what tenOever dubs “call to arms” genes and “call for reinforcement” genes.

      Support STAT: If you value our coronavirus coverage, please consider making a one-time contribution to support our journalism.
      The first group of genes produces interferons. These proteins, which infected cells release, are biological semaphores, signaling to neighboring cells to activate some 500 of their own genes that will slow down the virus’ ability to make millions of copies of itself if it invades them. This lasts seven to 10 days, tenOever said, controlling virus replication and thereby buying time for the second group of genes to act.

      This second set of genes produce their own secreted proteins, called chemokines, that emit a biochemical “come here!” alarm. When far-flung antibody-making B cells and virus-killing T cells sense the alarm, they race to its source. If all goes well, the first set of genes holds the virus at bay long enough for the lethal professional killers to arrive and start eradicating viruses.

      “Most other viruses interfere with some aspect of both the call to arms and the call for reinforcements,” tenOever said. “If they didn’t, no one would ever get a viral illness”: The one-two punch would pummel any incipient infection into submission.

      SARS-CoV-2, however, uniquely blocks one cellular defense but activates the other, he and his colleagues reported in a study published last week in Cell. They studied healthy human lung cells growing in lab dishes, ferrets (which the virus infects easily), and lung cells from Covid-19 patients. In all three, they found that within three days of infection, the virus induces cells’ call-for-reinforcement genes to produce cytokines. But it blocks their call-to-arms genes — the interferons that dampen the virus’ replication.

      The result is essentially no brakes on the virus’s replication, but a storm of inflammatory molecules in the lungs, which is what tenOever calls an “unique” and “aberrant” consequence of how SARS-CoV-2 manipulates the genome of its target.

      NEWSLETTERS
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      In another new study, scientists in Japan last week identified how SARS-CoV-2 accomplishes that genetic manipulation. Its ORF3b gene produces a protein called a transcription factor that has “strong anti-interferon activity,” Kei Sato of the University of Tokyo and colleagues found — stronger than the original SARS virus or influenza viruses. The protein basically blocks the cell from recognizing that a virus is present, in a way that prevents interferon genes from being expressed.

      In fact, the Icahn School team found no interferons in the lung cells of Covid-19 patients. Without interferons, tenOever said, “there is nothing to stop the virus from replicating and festering in the lungs forever.”

      That causes lung cells to emit even more “call-for-reinforcement” genes, summoning more and more immune cells. Now the lungs have macrophages and neutrophils and other immune cells “everywhere,” tenOever said, causing such runaway inflammation “that you start having inflammation that induces more inflammation.”

      At the same time, unchecked viral replication kills lung cells involved in oxygen exchange. “And suddenly you’re in the hospital in severe respiratory distress,” he said.

      In elderly people, as well as those with diabetes, heart disease, and other underlying conditions, the call-to-arms part of the immune system is weaker than in younger, healthier people, even before the coronavirus arrives. That reduces even further the cells’ ability to knock down virus replication with interferons, and imbalances the immune system toward the dangerous inflammatory response.

      The discovery that SARS-CoV-2 strongly suppresses infected cells’ production of interferons has raised an intriguing possibility: that taking interferons might prevent severe Covid-19 or even prevent it in the first place, said Vineet Menachery of the University of Texas Medical Branch.

      In a study of human cells growing in lab dishes, described in a preprint (not peer-reviewed or published in a journal yet), he and his colleagues also found that SARS-CoV-2 “prevents the vast amount” of interferon genes from turning on. But when cells growing in lab dishes received the interferon IFN-1 before exposure to the coronavirus, “the virus has a difficult time replicating.”

      After a few days, the amount of virus in infected but interferon-treated cells was 1,000- to 10,000-fold lower than in infected cells not pre-treated with interferon. (The original SARS virus, in contrast, is insensitive to interferon.)

      Related: Gilead ups its donation of the Covid-19 drug remdesivir for U.S. hospitals
      Ending the pandemic and preventing its return is assumed to require an effective vaccine to prevent infection and antiviral drugs such as remdesivir to treat the very sick, but the genetic studies suggest a third strategy: preventive drugs.

      It’s possible that treatment with so-called type-1 interferon “could stop the virus before it could get established,” Menachery said.

      Giving drugs to healthy people is always a dicey proposition, since all drugs have side effects — something considered less acceptable than when a drug is used to treat an illness. “Interferon treatment is rife with complications,” Menachery warned. The various interferons, which are prescribed for hepatitis, cancers, and many other diseases, can cause flu-like symptoms.

      But the risk-benefit equation might shift, both for individuals and for society, if interferons or antivirals or other medications are shown to reduce the risk of developing serious Covid-19 or even make any infection nearly asymptomatic.

      Interferon “would be warning the cells the virus is coming,” Menachery said, so such pretreatment might “allow treated cells to fend off the virus better and limit its spread.” Determining that will of course require clinical trials, which are underway.

      About the Author

      Sharon Begley
      Senior Writer, Science and Discovery

      Sharon covers science and discovery.

      sharon.begley@statnews.com
      @sxbegle
      Tags
      CORONAVIRUS
      INFECTIOUS DISEASE
      RESEARCH
      VIROLOGY
      Republish this article

    4. John Tooker on May 21, 2020 at 5:47 pm

      ‘It’s something I have never seen’: How the Covid-19 virus hijacks cells

      MAY 21, 2020

      ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI
      Adeep dive into how the new coronavirus infects cells has found that it orchestrates a hostile takeover of their genes unlike any other known viruses do, producing what one leading scientist calls “unique” and “aberrant” changes.

      Recent studies show that in seizing control of genes in the human cells it invades, the virus changes how segments of DNA are read, doing so in a way that might explain why the elderly are more likely to die of Covid-19 and why antiviral drugs might not only save sick patients’ lives but also prevent severe disease if taken before infection.

      “It’s something I have never seen in my 20 years of” studying viruses, said virologist Benjamin tenOever of the Icahn School of Medicine at Mount Sinai, referring to how SARS-CoV-2, the virus that causes Covid-19, hijacks cells’ genomes.

      The “something” he and his colleagues saw is how SARS-CoV-2 blocks one virus-fighting set of genes but allows another set to launch, a pattern never seen with other viruses. Influenza and the original SARS virus (in the early 2000s), for instance, interfere with both arms of the body’s immune response — what tenOever dubs “call to arms” genes and “call for reinforcement” genes.

      The first group of genes produces interferons. These proteins, which infected cells release, are biological semaphores, signaling to neighboring cells to activate some 500 of their own genes that will slow down the virus’ ability to make millions of copies of itself if it invades them. This lasts seven to 10 days, tenOever said, controlling virus replication and thereby buying time for the second group of genes to act.

      This second set of genes produce their own secreted proteins, called chemokines, that emit a biochemical “come here!” alarm. When far-flung antibody-making B cells and virus-killing T cells sense the alarm, they race to its source. If all goes well, the first set of genes holds the virus at bay long enough for the lethal professional killers to arrive and start eradicating viruses.

      “Most other viruses interfere with some aspect of both the call to arms and the call for reinforcements,” tenOever said. “If they didn’t, no one would ever get a viral illness”: The one-two punch would pummel any incipient infection into submission.

      SARS-CoV-2, however, uniquely blocks one cellular defense but activates the other, he and his colleagues reported in a study published last week in Cell. They studied healthy human lung cells growing in lab dishes, ferrets (which the virus infects easily), and lung cells from Covid-19 patients. In all three, they found that within three days of infection, the virus induces cells’ call-for-reinforcement genes to produce cytokines. But it blocks their call-to-arms genes — the interferons that dampen the virus’ replication.

      The result is essentially no brakes on the virus’s replication, but a storm of inflammatory molecules in the lungs, which is what tenOever calls an “unique” and “aberrant” consequence of how SARS-CoV-2 manipulates the genome of its target.

      In another new study, scientists in Japan last week identified how SARS-CoV-2 accomplishes that genetic manipulation. Its ORF3b gene produces a protein called a transcription factor that has “strong anti-interferon activity,” Kei Sato of the University of Tokyo and colleagues found — stronger than the original SARS virus or influenza viruses. The protein basically blocks the cell from recognizing that a virus is present, in a way that prevents interferon genes from being expressed.

      In fact, the Icahn School team found no interferons in the lung cells of Covid-19 patients. Without interferons, tenOever said, “there is nothing to stop the virus from replicating and festering in the lungs forever.”

      That causes lung cells to emit even more “call-for-reinforcement” genes, summoning more and more immune cells. Now the lungs have macrophages and neutrophils and other immune cells “everywhere,” tenOever said, causing such runaway inflammation “that you start having inflammation that induces more inflammation.”

      At the same time, unchecked viral replication kills lung cells involved in oxygen exchange. “And suddenly you’re in the hospital in severe respiratory distress,” he said.

      In elderly people, as well as those with diabetes, heart disease, and other underlying conditions, the call-to-arms part of the immune system is weaker than in younger, healthier people, even before the coronavirus arrives. That reduces even further the cells’ ability to knock down virus replication with interferons, and imbalances the immune system toward the dangerous inflammatory response.

      The discovery that SARS-CoV-2 strongly suppresses infected cells’ production of interferons has raised an intriguing possibility: that taking interferons might prevent severe Covid-19 or even prevent it in the first place, said Vineet Menachery of the University of Texas Medical Branch.

      In a study of human cells growing in lab dishes, described in a preprint (not peer-reviewed or published in a journal yet), he and his colleagues also found that SARS-CoV-2 “prevents the vast amount” of interferon genes from turning on. But when cells growing in lab dishes received the interferon IFN-1 before exposure to the coronavirus, “the virus has a difficult time replicating.”

      After a few days, the amount of virus in infected but interferon-treated cells was 1,000- to 10,000-fold lower than in infected cells not pre-treated with interferon. (The original SARS virus, in contrast, is insensitive to interferon.)

      Ending the pandemic and preventing its return is assumed to require an effective vaccine to prevent infection and antiviral drugs such as remdesivir to treat the very sick, but the genetic studies suggest a third strategy: preventive drugs.

      It’s possible that treatment with so-called type-1 interferon “could stop the virus before it could get established,” Menachery said.

      Giving drugs to healthy people is always a dicey proposition, since all drugs have side effects — something considered less acceptable than when a drug is used to treat an illness. “Interferon treatment is rife with complications,” Menachery warned. The various interferons, which are prescribed for hepatitis, cancers, and many other diseases, can cause flu-like symptoms.

      But the risk-benefit equation might shift, both for individuals and for society, if interferons or antivirals or other medications are shown to reduce the risk of developing serious Covid-19 or even make any infection nearly asymptomatic.

      Interferon “would be warning the cells the virus is coming,” Menachery said, so such pretreatment might “allow treated cells to fend off the virus better and limit its spread.” Determining that will of course require clinical trials, which are underway.

      About the Author

      Sharon Begley
      Senior Writer, Science and Discovery

      Sharon covers science and discovery.

      sharon.begley@statnews.com
      @sxbegle

      VIROLOGY
      Republish this article

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