Thread by @Marc_Veld

Prevalent and persistent new-onset autoantibodies in mild to severe COVID-19

Upon an immune response, antibodies reactive with self can be detected, SARS-CoV-2 is again no exception.


1/10nature.com/articles/s4146…

Infections are known to trigger flares of autoimmune diseases in humans. Infection-mediated autoimmune bystander (non-specific) and antigen-specific mechanisms can contribute to autoimmunity. Several publications have shown this is the same for SC2.


2/10sciencedirect.com/science/articl…

This paper shows that prevalent new-onset autoantibodies against a wide range of antigens can emerge following severe SARS-CoV-2 infection in pre-infectious baseline samples and remain elevated for at least 12 months.
Some have no resemblance to SC2 proteins, others do.
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There are no other infection controls: reducing conclusions about the specific effects of SC2 (see below).

The subjects included 32 healthcare workers (HCW) with self-reported symptoms post-COVID-19, and 16 hospitalized COVID-19 patients (severe).
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Important context: autoantibodies are generated with most if not all infections. Many of us have autoantibodies, the level of which increases with age. Autoantibodies do not mean autoimmune disease, most will have no clinical symptoms.


5/10sciencedirect.com/science/articl…

Do these antibodies matter? They probably increase the risk of autoimmunity, although their overall impact may be modest. There is no impact on mortality.

6/10academic.oup.com/rheumatology/a…

There is a hypothesis and substantiating data that some autoantibodies may play a role in some of the long-term effects of infection, such as ME/CFS and #LongCovid. Since these antibodies are generated upon inflammation, this can also happen after vaccination.
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Indeed, the authors confirm some symptoms correlate with particular antibody targets. This suggests that in some of us, cross-reactive (SC2 and self-protein), may contribute or cause longer-term symptoms. This part, the exact targets, is pathogen-specific.
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Important to know, that the more severe the disease, the higher the risk of making these antibodies. Immune memory from previous vaccination or infection will limit the inflammatory response required upon re-infection and reduce subsequent secondary risks.
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These autoantibodies are becoming a prime target and explanation for the diverse symptoms related to long-term post-infection effects, collectively called #Long COVID. Of note, they may be (temporarily) re-triggered upon re-infection or vaccination. That would be important.
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