Humoral immunity to an endemic coronavirus is associated with postacute sequelae of COVID-19 in individuals with rheumatic diseases, 2023,

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EndME

Senior Member (Voting Rights)
Humoral immunity to an endemic coronavirus is associated with postacute sequelae of COVID-19 in individuals with rheumatic diseases

Editor’s summary
It is not clear why some individuals develop postacute sequelae of COVID-19 (PASC) while others do not. Here, Herman et al. used systems serology to probe antibody features associated with development of PASC in individuals with rheumatic diseases. The authors found that the presence of functional antibodies specific to OC43, an endemic human coronavirus, were enriched in PASC. Although more causal analysis is warranted, these results suggest that immunological imprinting specific to OC43 may be a driver of PASC, particularly in individuals with prior rheumatic disease. —Courtney Malo

Abstract
Beyond the acute illness caused by severe acute respiratory coronavirus 2 (SARS-CoV-2) infection, about one-fifth of infections result in long-term persistence of symptoms despite the apparent clearance of infection. Insights into the mechanisms that underlie postacute sequelae of COVID-19 (PASC) will be critical for the prevention and clinical management of long-term complications of COVID-19.

Several hypotheses have been proposed that may account for the development of PASC, including persistence of virus and dysregulation of immune responses. Among the immunological changes noted in PASC, alterations in humoral immunity have been observed in some patient subsets.

To begin to determine whether SARS-CoV-2– or other pathogen-specific humoral immune responses evolve uniquely in PASC, we performed comprehensive antibody profiling against SARS-CoV-2, a panel of endemic pathogens, and a panel of routine vaccine antigens using systems serology in two cohorts of patients with preexisting systemic autoimmune rheumatic disease (SARD) who either developed or did not develop PASC. A distinct qualitative shift observed in Fcγ receptor (FcγR) binding was observed in individuals with PASC. Specifically, individuals with PASC harbored weaker FcγR-binding anti–SARS-CoV-2 antibodies and stronger FcγR-binding antibody responses against the endemic coronavirus OC43. Individuals with PASC developed an OC43 S2-specific antibody response with stronger FcγR binding, linked to cross-reactivity across SARS-CoV-2 and common coronaviruses.

These findings identify previous coronavirus imprinting as a potential marker for the development of PASC in individuals with SARDs.

https://www.science.org/doi/10.1126/scitranslmed.adf6598
 
 
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You beat me to it @EndME !

Also in A common allele of HLA is associated with asymptomatic SARS-CoV-2 infection (2023, Nature) —

This observation is in accordance with previous research in uninfected HLA-B*07:02 + individuals who are able to recognize the N(105–113) peptide derived from SARS-CoV-2 due to the presence of cross-reactive T cells recognizing the homologous N(105–113) peptide from OC43-CoV and HKU1-CoV. Notably, this T cell cross-reactivity has been associated with less severe COVID-19 disease.
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Additionally, we've had unbalanced cellular/humoral immune responses noted in LC, eg —

Divergent adaptive immune responses define two types of long COVID (2023, Frontiers in Immunology)
Long COVID manifests with T cell dysregulation, inflammation, and an uncoordinated adaptive immune response to SARS-CoV-2 (2023, Preprint: BioRxiv)

And immunoglobulin class switching dependent on prior infection and vaccination history —

Class switch towards spike protein-specific IgG4 antibodies after SARS-CoV-2 mRNA vaccination depends on prior infection history (2023, Nature Scientific Reports)
Class switch toward noninflammatory, spike-specific IgG4 antibodies after repeated SARS-CoV-2 mRNA vaccination (2022, Science Immunology)
 
A while back we looked at a paper on immune memory in relation to viruses, which we thought might be relevant to ME but I haven't been able to find the thread again.
 
I haven't looked at the exact cohorts yet. It would be interesting to know whether any patients were taking immunosuppressants to treat RA during their acute infection. Very broadly speaking I would think that those that are immunocompromised would be more likely to develop a persistent virus. Whilst it is true for the acute infection, which can often last weeks or months in these patients, immunocompromised patients very seldomly develop LC, at least not more often than young and healthy people.
 
NIH wrote a news article about it.


Cold virus may set the stage for Long COVID
https://www.nih.gov/news-events/nih-research-matters/cold-virus-may-set-stage-long-covid

Many infections with SARS-CoV-2, the virus that causes COVID-19, resolve within days or weeks. But a significant number of people have symptoms that linger for weeks, months, or even years. This is called postacute sequelae of COVID-19 (PASC)—commonly known as “Long COVID.” While several risk factors for PASC have been proposed, we still don’t understand what causes it or why some people get it and others don’t. To further complicate matters, PASC may have different causes in different people.
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The findings suggest that PASC may arise from a phenomenon known as immune imprinting. This refers to how a person’s history of previous infections can affect their immune response to new infections. In this case, when a person who was previously exposed to OC43 is infected with SARS-CoV-2, their immune system responds partly by using antibodies developed during OC43 infection that also recognize SARS-CoV-2. This “recall” response to OC43 leads to an inefficient overall response to SARS-CoV-2. Further research will be needed to determine if and how this weak immune response may lead to PASC.​
 
From the article:
Some with PASC have changes in certain immune responses, suggesting an immune mechanism for PASC. PASC is particularly common among people with systemic autoimmune rheumatic diseases. These are chronic diseases, such as lupus, where the immune system mistakenly targets the body’s own tissues to cause inflammation. Up to 45% of those with these rheumatic diseases who are infected with SARS-CoV-2 develop PASC.
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