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Article: "Zombie" viral fragments trigger inflammation to cause serious COVID-19 outcomes
Study: Viral afterlife: SARS-CoV-2 as a reservoir of immunomimetic peptides that reassemble into proinflammatory supramolecular complexes
Whether these SARS-CoV-2 fragments imitating peptides from the innate immune system might be playing a role in long COVID ME/CFS, the study did not say.
The research team found SARS-CoV-2 fragments can imitate innate immune peptides, a class of immune molecules that amplify signals to activate the body's natural defenses.
Study: Viral afterlife: SARS-CoV-2 as a reservoir of immunomimetic peptides that reassemble into proinflammatory supramolecular complexes
Discussion
We have shown that an unanticipated mechanism for propagating inflammation through uninfected cells exists for SARS-CoV-2 but not for common cold coronaviruses. This mechanism involves viral fragments able to mimic AMPs like LL-37 cathelicidin in host innate immunity.
Given that LL-37 is involved in pathogenesis of lupus and rheumatoid arthritis, the notion that SARS-CoV-2 peptide fragments can imitate LL-37 may be conceptually salient for understanding why the immune systems of COVID-19 patients resemble those of people with autoimmune disorders like lupus and rheumatoid arthritis
Whether these SARS-CoV-2 fragments imitating peptides from the innate immune system might be playing a role in long COVID ME/CFS, the study did not say.
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