Detection of herpes viruses in patients with myalgic encephalomyelitis /chronic fatigue syndrome in Belarus, 2020, Orlova et al

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Detection of herpes viruses in patients with myalgic encephalomyelitis /chronic fatigue syndrome in Belarus

Svetlana Orlova, Galina Rudjko, Olga Orlova, Tatsiana Dakukina

Abstract
Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a multifactorial chronic disease. The etiology and pathogenesis of ME/CFS are unknown . There are many theories for the occurrence of this disease. but the most convincing is the infectious or viral theory of the emergence of CFS.

The aim of this study is to detect of herpes viruses 6, 7 types and Epstein-Barr to examine the prevalence HHV-6, HHV-7 and EBV infections in Belarus CFS patients .

We examined 30 patients with CFS in whom fatigue during more than 2 years (7), more than 1 year (11) and more than 6 months (12). The diagnosis was made on clinical grounds using the Fukuda criteria.

The presence of markers the active forms infection HHV-6 and HHV-7 in CFS patients with a long period of fatigue were detected in 16.6% and 26.6% respectively. IgM antibodies to HHV-6 and EBV. positive, in 16.6% and 6.7% respectively in patients with long-term illness. Detection of IgG antibodies indicates a quiet carrier state, latent phase.

Link | PDF (Polish Journal of Applied Sciences) [Open Access]
 
This rings a bell from a while ago considering it was published in 2020. Pol. J. Appl. Sci., 2020, 6, 50-5

I think they are summarising several experimental passes of divided stored samples at different times, otherwise I find it impossible to reconcile statements as follows.
Viremia HHV-7 was detected in 26.6%
...
viremia of either both viruses or one was in 4 patients

26.6% is 8 patients out of 30 so these must have been different experiments because the second statement refers to patients with both HH6 and HH7. If 8 patients have HH7 viremia then the total with viremia in the second ought not be less than 8. Possibly a second set of tests did not detect what the first set did? It is not explained. Implies inconsistency possibly due to time sensitivity of samples and tests.

"stored at 40–80ºC" looks like a typo.

Thirty patients with ME/CFS (23 females, 7 males), and 20 randomly selected blood donors (10 females, 10 males) as controls (cohort compared ) were investigated

stark contrasts with controls, especially HH7 but none are ubiquitous

ConclusionPost-infection chronic fatigue syndrome is usually observed in patients in six or more months after the end of an acute viral infection. The presence of markers the active forms infection HHV-6 and HHV-7 in CFS patients with a long period of fatigue were detected in 16.6% and 26.6% respectively. This may be the result of reactivation of viruses under the influence of various provoking factors.
...
The high incidence of HHV-6 HHV-7 and EBV in CFS patients suggests that they may be markers and trigger factors for the development of CFS.

'may' being the important word.

IMHO based on my own experience, these may also represent opportunist infections proliferating due to an immune system failure associated with another cause, such as a previous infection by a different virus.

Though none of the tested viruses are ubiquitous in ME/CFS patients, some might yet be triggers if several different viruses can trigger ME/CFS, which is possible because convergent evolution of viruses to disable the immune system, e.g. TAP system, has also been documented. Besides which many of these viruses belong the same taxon of herpes viruses meaning they may have inherited this putative ability.

https://en.wikipedia.org/wiki/Transporter_associated_with_antigen_processing

I wrote a blog about it a while ago in the hope the boffins would be well and truly ninjad because I am fed up of waiting. :sneaky::ninja:

https://boolyblog.blogspot.com/2014/05/why-viruses-immunoevasins-and-mixed.html

But it is not necessarily TAP evasion which causes ME, it might be but there might be other immunoevasion strategies out there which do. The point is if there is a weakness, viruses will convergently evolve to exploit it. So it is within the bounds of credibility for there to be many different trigger infections for ME all attacking the same weakness and causing similar kinds of immune failure.
 
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