Michael Hunter, MD on Medika Life

Why Covid Hits Some Hard

WHY DOES COVID-19 WREAK SUCH DESTRUCTION on some individuals and not others? Race appears to play a role, as do age and other medical conditions such as obesity, high blood pressure, and heart problems. Active cancer treatment such as chemotherapy can make one more vulnerable, too. I would be remiss if I did not mention vaccination status.

But what tips an individual into life-threatening severe pneumonia, also known as acute respiratory distress syndrome, or ARDS? I want to share with you some possibilities, as nicely articulated in a piece from the University of California, San Francisco (USA).

“Chaos was the law of nature; Order was the dream of man.”
― Henry Adams, The Education of Henry Adams

Ariel Bleicher begins with this observation: “What we still don’t know, however, is what tips one COVID-19 victim toward ARDS but not another.” Moreover, those with the novel coronavirus had a peculiar clinical course compared with those with ARDS who did not have the virus.

Those harboring COVID-19 developed the syndrome more slowly and typically recovered more slowly as well. Their immune system goes on a rampage, one against its own body, wreaking havoc on the lungs and depriving them of vital oxygen. This process continues even after COVID-19 has cleared out.

But COVID-19 does not limit itself to the lungs. The virus can also attack our heartgutbrain, blood vessels, and more. Like in the lungs, the patients’ immune response can be more problematic than the direct damage caused by the virus. Inflammation abounds.

I have recently written about how COVID-19 microclots may play a role in facilitating long-term symptoms from the infection, a phenomenon colloquially referred to as long COVID:Long Covid: Could This Be Why?MICROCLOTS. COULD THEY EXPLAIN the mystery of why some who get a COVID19 infection suffer for long periods? Three…medium.com

COVID-19 unhinges the immune system

We next turn to the COMET (COVID-19 Multi-Phenotyping for Effective Therapies), a study that collects blood and other body substances from the hospitalized patient for genes, immune cells, and other molecules.

Researchers sequenced RNA, indicating which genes (DNA) are activated. In this fashion, they could see what genetic programs a patient’s immune cells used in response to the COVID-19 infection.

Here are the findings:

Immune cells from patients with mild COVID-19 ran a crucial virus defense program without a problem. On the other hand, those with severe COVID-19 (admitted to the ICU, often with ARDS) had no cells running an essential response centered around interferon.

Photo by Patrick Robert Doyle on Unsplash

Bleicher breaks it down. Our immune cells deploy several programs to combat viruses. A potent one is the interferon response. We have some immune cells that are sentries at our borders, including in the skin and the lining of our noses.

When one of these sentinel soldier cells detects a virus attack, it releases warning proteins — interferons — as a siren. Cells in the vicinity respond by activating anti-viral genes, slowing the reproduction of the virus. The genetic activation also promotes cell suicide among the cells that have become infected.

Professor Matthew “Max” Krummel, Ph.D., UCSF’s Smith Professor of Experimental Pathology, and co-lead of the COMET study, explains that we see this lack of an interferon response unfold across the entire immune system.

Cytokine storm

With no interference response to contain the virus, the COVID-19 invader spreads freely and rapidly. As the virus attacks more and more cells, the cells call for reinforcements by releasing inflammatory proteins (cytokines) into the bloodstream.

Things heat up even more as white cells and antibodies join the war, striving to eliminate the COVID virus via biological carpet bombing. Perhaps not surprisingly, extensive inflammation and tissue damage ensues.

What’s shutting down the interferon response?

Approximately ten percent of those with severe COVID-19 have antibodies in their blood that attack interferons. For others with severe infections, there may be a host of yet discovered antibodies binding to a cell receptor that overrides the interferon signal.

The researchers came to this unbelievable conclusion: Hidden autoimmunity may turn an otherwise benign infection deadly. And antibodies against interferon may be the tip of the iceberg. As we learn more about antibodies and their effect on COVID-19, we are likely to understand better who is more likely to become severely ill.

Thank you for joining me in exploring this exciting research.


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Michael Hunter, MD
Michael Hunter, MD
I received an undergraduate degree from Harvard, a medical degree from Yale, and trained in radiation oncology at the University of Pennsylvania. I practice radiation oncology in the Seattle area.

Michael Hunter, MD

I received an undergraduate degree from Harvard, a medical degree from Yale, and trained in radiation oncology at the University of Pennsylvania. I practice radiation oncology in the Seattle area.

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