Survey of Anti-Pathogen Antibody Levels in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome, 2022, Levine,Hanson et al

Sly Saint

Sly Saint

Senior Member (Voting Rights)
Abstract
Infectious pathogens are implicated in the etiology of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) because of the occurrence of outbreaks of the disease. While a number of different infectious agents have been associated with the onset of ME/CFS, the identity of a specific organism has been difficult to determine in individual cases. The aim of our study is to survey ME/CFS subjects for evidence of an infectious trigger and/or evidence of immune dysregulation via serological testing of plasma samples for antibodies to 122 different pathogen antigens. Immune profiles were compared to age-, sex-, and BMI-matched controls to provide a basis for comparison. Antibody levels to individual antigens surveyed in this study do not implicate any one of the pathogens in ME/CFS, nor do they rule out common pathogens that frequently infect the US population. However, our results revealed sex-based differences in steady-state humoral immunity, both within the ME/CFS cohort and when compared to trends seen in the healthy control cohort. View Full-Text

https://www.mdpi.com/2227-7382/10/2/21
 
5. Conclusions
While examining levels of antibodies to whole proteins and lysates would not be expected to identify a disease-causing pathogen specific to ME/CFS if the pathogen routinely affects large numbers of individuals, rare pathogens could be implicated if they are found to be more prevalent in the case group. Although some rare pathogens were probed in our study, none show significant differences between cases and controls after false discovery rate correction. To the best of our knowledge, this is the first time that antibody levels to many of the pathogens investigated here have been explored in ME/CFS patients, including tick-borne encephalitis virus, hepatitis E virus, and human metapneumovirus. We also probed the largest number of adenoviruses (14) and enteroviruses (20, in five different groups) of any study to date. While the primary conclusion from our study is the absence of differences between antibody levels of patients and controls, this type of exploratory analysis using high-throughput, multiplex technologies is important to characterize the humoral immune response of ME/CFS patients and to continue the search for a possible infectious agent that triggers ME/CFS. We also show a trend in male antibody levels suggesting immunosuppression as well as differences in antibody levels with age. The subtle serological alterations between healthy controls and ME/CFS subjects found here should be interpreted cautiously, but these findings do contribute to the growing body of evidence that the immune system of ME/CFS patients is dysregulated [32,36]. We also recommend that future serological studies in ME/CFS patients should not combine males and females for analysis and that males should be studied in addition to females despite being a smaller subset of the patient population.
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I am interpreting this to show that exposure to any of specific pathogens investigated is not sufficient or necessary to trigger ME/CFS though we can not rule that exposure to one or more of a number of pathogens is a contributory factor in the genesis of the condition.

Though we are left with a theoretical possibility that an as of yet unidentified pathogen is responsible, most people will still assume that the condition can be triggered to varying degrees by any of a range of pathogens in individuals that somehow are at that point in time susceptible.

This does does leave open the need to investigate whether the apparent phenomenon that some viruses are more likely to trigger ME than others (eg EBV or Covid-19) is real and helpful in understanding the condition.

[sorry went on drafting this comment after I had posted it without realising that was what I was doing]
 
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I have not read the paper so I don't know if they controlled for this.

Polio was caused by an abnormal response to a fairly common infection. In 1984 people felt that ME could be caused by an abnormal response to a common coxsackie or other enteroviral infection. Some people believe they get ME from an abnormal response to an EBV infection.

Long ago I spoke to a researcher who said that enteroviruses did not cause ME because everyone had antibodies as such infections are so common. He did not seem to know about polio.

There may well be some common factor why common infections lead to ME but I am not convinced antibody studies will help.

Also, if it is a rare infection would I still have measurable antibody levels after 58 years?
 
Yes, it might be better stated that some people have unusual sequelae to common infections :)

When I became ill my uncle did too. He experienced recurrent kidney infections for over 10 years and has been well since. Many people report that a few people who work together or are relayed become sick at the same time and most of the group recover.
 
I am a little concerned about their assumptions and inferences (and I'm a fan of this tandem +). Then again, I'm unclear about some specifics. Could they break out individual vs pooled? I apologize if I missed or forgot that.

Main assumption that gnaws at me: Why assume a pathogen is not at play simply because you find antibodies to it at similar levels in healthy controls - in plasma?

Edit to add: If we are going to get serious about pathogen hunting, then we need to be looking at tissue.
 
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