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An article was published yesterday in Frontiers in Immunology entitled “Myalgic Encephalomyelitis / Chronic Fatigue Syndrome: the biology of a neglected disease.” ME/CFS is on ohm’s disease list.

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Every study I've ran across has shown it to be an immune dysfunction/inflammatory disease.

From the article -
https://www.frontiersin.org/journals/immunolo...86607/full

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Some polymorphisms in genes related to the immunomodulatory response have been identified, such as an increase of TNF-857 TT and CT genotypes (p=0.002), and a significant decrease of IFN gamma low producers (A/A) (P=0.04) in ME/CFS patients in respect to controls. Polymorphisms impacting hormone action have also been noted . For example, NR3C1-1F DNA methylation was found reduced in patients with ME/CFS

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Increase in TNF and less patients that have low IFNy low production. Both controlled by leronlimab. There are no direct studies of NR3C1-1F and CCR5 but low NR3C1-1F leads to an increase in a large host of inflammatory factors that leronlimab downregulates. Genetic NR3C1-1F polymorphisms are also implicated in depression, bi-polar disorder and PTSD.

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HLA proteins are crucial for the immune system as they distinguish foreign pathogens from self-cells. An increased frequency of HLA-DQA1 alleles and reduced expression of HLA-DRB1 was found associated with ME/CFS

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Those genetic alterations are implicated in autoimmune diseases.

Genetic alterations like these and others (or the lack thereof) may be the reason why there some non-responders in the Long Covid and other trials. Fairly large scale trials would be necessary to make the determination of which genetic anomalies reduce leronlimab's performance.

The next section looks at reactivation of dormant viruses. I didn't read it but here's my take. Dormant viruses are going to reactivate when the immune system is stressed. That can be due to other viral or bacterial infections, other disease states and intense physical trauma. EBV or other dormant infections are not the cause of ME/CFS or Long Covid they are just a hallmark of the underlying pathology of immune dysfunction/inflammation.

Of course with that immune overreaction you're going to see all of those inflammatory cytokines and increased activity of macrophages and microglia. As we know that can lead to neurological and physical damage. It all leads back to the CCR5 receptor. Since I didn't read the entire article, just for the hell of it I did a search for CCR5. Alas, not a single mention.