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Big news: severe COVID linked to auto-antibodies to type 1 interferons

coronavirus

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#1 geo12the

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Posted 25 May 2022 - 04:53 AM


On the latest TWIV (this week in virology) podcast they went over a just published paper that seems to uncover the mode of action of why some people get severe COVID and die.

Link is here.

 

It hasn't hit the news yet, I guess there is more important stuff like the Johnny Depp trial LOL,  but it seems like this study is very significant in our understanding of why COVID kills some people. To sum it up as best I can, people with auto antibodies against Interferon alpha and omega, are much more likely to die from COVID. And as people age they become more likely to have these autoantibodies. Interferons are proteins made by the body that mobilize defense against viruses. People with these auto-antibodies make much less of them so are not able to fight off the virus as well. I think this paper opens up whole new avenues for screening people to determine who is more likely to die from COVID and for developing targeted therapeutics. From the discussion of the paper:

 

"auto-Abs against type I IFNs should be considered as a leading common predictor of life-threatening COVID-19, after age, as their detection appears to have a much greater predictive value for death, and, by inference, hospitalization and critical COVID-19, than sex, comorbidities, and common genetic variants"

 

Full link to the study in PNAS: 

 

 

The risk of COVID-19 death is much greater and age dependent with type I IFN autoantibodies

 

  


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#2 Hip

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Posted 28 May 2022 - 04:08 AM

That interesting. Though if type 1 interferon autoantibodies are impeding the interferon immune response in these more severe COVID cases, you would have thought that interferon therapy would help rectify this problem.

 

However, according to this article, interferon therapy has not benefited COVID patients.


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#3 geo12the

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Posted 29 May 2022 - 04:33 PM

That interesting. Though if type 1 interferon autoantibodies are impeding the interferon immune response in these more severe COVID cases, you would have thought that interferon therapy would help rectify this problem.

 

However, according to this article, interferon therapy has not benefited COVID patients.

 

I am not sure but could have to do with specificity. The correlation in the paper between severe COVID and interferons was specific to autoantibodies against IFN-α2 or IFN-ω. I am not an expert in this field but from what I have read therapies using interferons more frequently use IFN-β. In the article you cite they say: " In a large randomized controlled trial of hospitalized patients with COVID-19, the combination of interferon beta-1a plus remdesivir showed no clinical benefit when compared to remdesivir alone". In the article I cite they say beta does not have a strong correlation to severity:  "auto-Abs neutralizing IFN-β were less common, and associated with lower RRD (relative rate of death)". 







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