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Researchers find yet another way to potentially explain long COVID and perhaps other post-infectious illnesses

coronavirus antibodies

This study assessed levels of antibodies to the current coronavirus and past ones.

One outcome of more or less abundant funding and the worldwide reach of COVID-19 is the creativity that gets unleashed. This Harvard study “Impact of cross-coronavirus immunity in post-acute sequelae of COVID-19did something that’s never been tried in chronic fatigue syndrome (ME/CFS) but presents some intriguing possibilities for it as well.

Taking advantage of the fact that antibodies can also be used as indirect markers of historical infections, the study “deeply explored alterations” in the antibody response as well as to related coronaviruses and a host of other pathogens in 43 people with rheumatological diseases such as rheumatoid arthritis and psoriatic arthritis (but not fibromyalgia). The goal was to see if the findings shed light on why some people came down with post-acute sequelae of COVID-19 (PASC), e.g. long COVID, and others didn’t.

Antibodies to the following infections and vaccines were assessed:

Vaccine antigens (Tetanus, Rubella, Measles, Mumps), herpesviruses (herpes simplex 1 – HSV-1, cytomegalovirus -CMV, Epstein Barr virus -EBV, Varicella Zoster virus – VZV), other coronaviruses (SARS-CoV-1 Spike/S1/S2, OC43 Spike/S1/S2, HKU1 Spike/S1/S2) and other human-infecting pathogens (Influenza, Respiratory Syncytial virus (RSV), and Staphylococcus aureus) and control pathogens (Ebola).

From Bruce Patterson’s monocytes, to the “original antigenic sin”, to persisting viruses or pieces of viruses, to micro clots, platelet hyperactivation, and amyloid fragments, long-COVID research is opening up new opportunities to understand it and other post-infectious illnesses such as ME/CFS.

The Gist

  • Long COVID research opens yet another new and different possibility for post-infectious illnesses. 
  • Harvard researchers went beyond normal antibody testing to assess antibodies for the SARS-CoV-2 coronavirus, for a coronavirus that causes the common cold, and for a number of other pathogens in long COVID patients and in recovered COVID-19 patients with pre-existing rheumatological diseases. 
  • The people with long COVID displayed a distinct antibody pattern: antibodies to the coronavirus causing the common cold were elevated, while antibodies against the SARS-CoV-2 virus that sparked the current pandemic were reduced.  Plus the elevated antibodies were triggering an inflammatory response. 
  • This indicated that something called “an original antigenic sin” or “immune imprinting” had occurred. This occurs when the immune system dredges up an older and less effective immune response to a similar pathogen to fight a new pathogen. This results in the immune system being “trapped” and unable to mount an optimal response.
  • The authors proposed that this deficient immune response may have caused the immune systems of people with long COVID to fail to clear the virus, leaving either it or the proteins associated with it, to persist – causing an ongoing immune reaction and inflammation. This process has never been assessed in ME/CFS.
  •  Viral persistence has been proposed in ME/CFS/FM, and some evidence of viral persistence has emerged in long COVID. The Long COVID Research Foundation – which has strong ME/CFS roots – is devoting substantial resources to see if viral persistence is present  and causing problems in long COVID. If so, it has pledged to work on ME/CFS next. 
  • From Bruce Patterson’s monocytes, to the “original antigenic sin”, to persisting viruses or pieces of viruses, to micro clots, platelet hyperactivation, and amyloid fragments, long-COVID research is opening up new opportunities to understand it and other post-infectious illnesses such as ME/CFS.

Results

Lo and behold, the people with long COVID or PASC, and the people who’d recovered from COVID-19, displayed significantly different antibody profiles. People with long COVID displayed significantly enriched or elevated levels of a cytomegalovirus (CMV) antibody and a coronavirus antibody associated with the common cold (OC43 Spike-specific FcγR3a/3b).

The CMV enrichment was a false lead, as more people with PASC had been infected with CMV in the past, but the high levels of antibodies to the spike protein of OC43 – a common cold coronavirus in the same lineage as the SARS-CoV-2 coronavirus – raised some eyebrows. That prompted a search to see if the antibody response to the coronavirus that caused the common cold had impacted the antibody response to the SARS-CoV-2 coronavirus that’s swept the world.

First, they found that the common cold antibody response was likely triggering inflammation. The antibodies found recruit neutrophils to sites of inflammation and activate them – suggesting that a dramatic increase in inflammation had occurred.

Plus, the overall antibody response (OC43-specific FcγR2a, FcγR2b, FcγR3a) to the common cold coronavirus ratcheted up – indicating that the long-COVID patients’ immune systems reacted to the new coronavirus by dredging up a response to its less dangerous cousin. This coincided with an inhibited antibody response to the current SARS-CoV-2 coronavirus. Not only that, but this antibody switch appeared to turn on an inflammatory response as well.

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Original Antigenic Sin 

This process – called the “original antigenic sin”, “immune imprinting”, or the Hoskins effect, has been called “the downside of immunological memory“. It occurs when instead of creating a new immune response that specifically targets the current pathogen, the immune system dredges up an older and less effective immune response to a similar pathogen. This results in the immune system being “trapped” and unable to mount an optimal response when confronted with a new virus.

It’s been known to occur with influenza, HIV, dengue fever, and other viruses, and was found to occur in some hospitalized COVID-19 patients last year. The impact of this “back-boosting” or “immune imprinting” attempt by the immune system to fight the coronavirus is unclear. This study, though, suggests it may be unhelpful, indeed, as an “immune imprinting” response was associated with long COVID in this patient group.

Viral Persistence Explained?

Coronavirus persistence

An inadequate antibody response to the SARS-CoV-2 virus might be allowing it to persist.

The authors noted that this strange immune response could explain why either the spike protein or the SARS-CoV-2 virus itself may persist in people with long COVID. The inability of the long-COVID patients’ body to mount a strong immune response that’s specific to the new coronavirus may cause the virus in one form or another to remain.

A new and quite different immune hole from what we’ve seen in ME/CFS has been uncovered and the specter of viral persistence raises its head again. Could a combination of imprinted immunity / viral persistence also be opening the door to ME/CFS in some people?

Some evidence of viral persistence in long COVID has emerged. Bruce Patterson has evidence indicating that SARS-CoV-2 proteins may be sparking an ongoing immune response in long COVID. Another study found residual virus in appendix, skin, and breast tissues of 2 long-COVID patients. Other studies have found it in the gut, plasma, and stool. One case report brought a possible new treatment approach to bear when it found nirmatrelvir/ritonavir and tocilizumab treatment reduced symptoms in a long-COVID patient with coronavirus persisting in her throat.

Health Rising recently reported on a major new effort from the Long COVID Research Foundation – which has strong ME/CFS roots – to determine whether viral persistence plays a major role in long COVID. If viral persistence is found, PolyBio has pledged to look for it in ME/CFS.

Lighting a Spark: Major New Long-COVID Initiative Promises Rapid Movement

From EBV and herpes zoster to enteroviruses, viral persistence and reactivation has been something of a theme in ME/CFS/FM, yet aside from Dr. Chia’s and Dr. Pridgen’s gut samples, it has been little addressed. Should viral persistence be shown to play a role in long COVID, it will surely be addressed in ME/CFS as well.

Whatever the answer ultimately turns out to be, long COVID is doing what we hoped it would do – bring new and creative approaches to the study of post-infectious illnesses. From Bruce Patterson’s monocytes, to the “original antigenic sin”, to persisting viruses or pieces of viruses, to micro clots, platelet hyperactivation, and amyloid fragments, long-COVID research is opening up new opportunities to understand it and other post-infectious illnesses such as ME/CFS. 

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