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Defining post-acute COVID-19 syndrome (PACS) by an epigenetic biosignature in peripheral blood mononuclear cells (Nikesjo et al, 2022)

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Abstract

Post-acute COVID-19 syndrome (PACS) has been defined as symptoms persisting after clearance of a COVID-19 infection. We have previously demonstrated that alterations in DNA methylation (DNAm) status persist in individuals who recovered from a COVID-19 infection, but it is currently unknown if PACS is associated with epigenetic changes. We compared DNAm patterns in patients with PACS with those in controls and in healthy COVID-19 convalescents and found a unique DNAm signature in PACS patients. This signature unravelled modified pathways that regulate angiotensin II and muscarinic receptor signalling and protein–protein interaction networks that have bearings on vesicle formation and mitochondrial function.

https://clinicalepigeneticsjournal.biomedcentral.com/articles/10.1186/s13148-022-01398-1
 
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Quote from the paper

We found a tendency of increased levels of CHRM3-specific IgG autoantibodies in our PACS cohort. Functionally active auto-antibodies are known to disturb the balance of neuronal and vascular activity and in fact, extracorporeal apheresis could reduce levels of autoantibodies and alleviate symptoms of CFS in a recent PACS study [9]. The finding of epigenetic modulation of the pathways of the same receptors for which auto-antibodies are described in PACS and CFS is intriguing and raises the question of a possible mechanistic relationship. Hypothetically, as part of the anti-viral defense, the host could down-modulate (either by creating autoantibodies or epigenetically) pathways exploited by the virus, which when they become persistently downregulated after viral clearance, may contribute to impairment of cellular functions. In line with this idea, the PPI modules that we found to be epigenetically modulated include cellular processes that are central to vesicle formation, exemplified by the identified connection of PACSIN2 and sub-membrane actin remodeling (ARP2/3), which potentially contributes to the formation of new virus particles. Another identified module with very strong interactions with SARS-CoV-2 involves NDUFA proteins, which regulate the NADH oxidase in mitochondria. Mitochondrial dysfunction was recently described in PACS [10] and our finding of an epigenetically modified module at the core of mitochondrial function warrants further investigation in PACS.
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Sounds like a chronic anti-viral state where the body is trying to deplete the virus of resources but at a cost to self.
 
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