Cytomegalovirus, Epstein‐Barr Virus and Human Herpesvirus 6 Infections in Patients with [ME/CFS], 2020, Shikova et al

Andy

Andy

Retired committee member
Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a disabling multisystem chronic disease. The etiology and pathogenesis of ME/CFS are unknown. Infections of cytomegalovirus (CMV), Epstein‐Barr virus (EBV) and human herpesvirus‐6 (HHV‐6) are suspected as etiological agents for ME/CFS.

This study aims to estimate prevalence and type (active/latent) of EBV, CMV and HHV‐6 infections in Bulgarian ME/CFS patients. In the study were included 58 ME/CFS patients and 50 healthy controls. Virus‐specific antibodies were detected by ELISA and viral genomic sequences in PBMCs and plasma samples ‐ by nPCR. We did not observe any significant differences in virus specific IgG and IgM positivity rates between ME/CFS patients and control group. In ME/CFS plasma samples EBV DNA was found in 24.1%, CMV DNA – in 3.4% and HHV‐6 DNA in 1.7% of samples. EBV DNA was detected in 4%, CMV and HHV‐6 DNA were not found in plasma samples of controls. The frequency of viral genome detection in PBMCs of patients and controls was 74% vs 78% for CMV, 81% vs 84% for EBV, and 82.8% vs 82% for HHV‐6. The difference in frequency of EBV active infection in ME/CFS and control group was statistically significant (p=0.0027). No ME/CFS and control individuals with active CMV and HHV‐6 infection were observed.

In conclusion, our study using both serological and PCR‐based techniques for distinguishing between active and latent infection, showed high rate of active EBV infection among ME/CFS patients indicating that at least in a subset of cases EBV is important factor for development of disease.
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Paywall, https://onlinelibrary.wiley.com/doi/pdf/10.1002/jmv.25744
Not available via Sci hub at time of posting.
 
This is a paper by one of the EUROMENE working groups. You would think that, by now, they would have realized that ME/CFS research requires innovative ideas rather than repeating the same old studies. Replicating results from studies proposing a potential biomarker is definitely important, but not looking yet again at EBV, CMV and HHV6...

I'm very disappointed by EUROMENE. 4 years of existence without a single viable result yet.

Off-topic: I still haven't quite gotten over this bit from their "Investigating care practices pointed out to disparities in diagnosis and treatment across European Union" paper yet, which I assume Elin Strand may have insisted on adding as she was the lead author (bolding mine):
Discussion (p. 8) said:
Both CBT and GET are controversial, and there are disagreements and uncertainty among both patients and health providers regarding the effect of the methods. That these approaches are used as treatment and self-management strategies in ME/CFS patients may imply that even if they do not cure, they are experienced as helpful by both health-providers and patients.
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For many years ME was associated with enteroviruses but no one seems to acknowledge that nowadays. They may not be the only cause but neglecting that aspect could be why we don't make much progress.

It is like residents complaining about a road junction and the authorities looking at the wrong one then saying their complaints have no basis.
 
showed high rate of active EBV infection among ME/CFS patients indicating that at least in a subset of cases EBV is important factor for development of disease.
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Uhh... wrong no wrong. Nothing proven in this paper regarding development of disease. All they’ve shown is higher EBV activity is associated with having ME/CFS. Given all the mountains of conflicting evidence showing no real connection to herpes viruses, it’s much more likely that the underlying core ME pathology is causing increased activity, not the reverse.
 
leokitten said:
Uhh... wrong no wrong. Nothing proven in this paper regarding development of disease. All they’ve shown is higher EBV activity is associated with having ME/CFS. Given all the mountains of conflicting evidence showing no real connection to herpes viruses, it’s much more likely that the underlying core ME pathology is causing increased activity, not the reverse.
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EBV is epstein-barr not herpes. I am not sure I understand what you are saying? Why is it more likely that the underlying core is causing increased activity than the reverse? I am seriously curious.
 
90 percent of people have antibodies to EBV as they get older so it is very common and like all herpes viruses the actual virus remains in the body but it locked away. Think of the way that chicken pox can cause shingles 60 years after the initial infection. herpes virus reactivation could be the cause of a lot of diseases.

During the epidemic which gave rise to the concept of CFS, they initially thought it was EBV so Stephen Strauss, whose speciality was chronic EBV, was brought in by the CDC to oversee things. He saw this epidemic as vindicating a lot of his theories. When it was found that many of the patients were negative for the virus he was not pleased. The original definition of CSF was simply the symptoms of chronic EBV with the need to be positive for the virus removed.

Strauss was horrible and a lot of our woes are down to him. He refused to listen to the ME experts who said this was another epidemic of ME and probably associated with enteroviruses so they walked out in protest - a mistake they regretted.

The confusion brought in then is still with us. Reactivated EBV may well be causing many of the symptoms of ME rather than being the primary cause. Every virus takes a certain time to spread and produce symptoms, it is like a fingerprint so EBV could not have been the cause during the epidemics.

Since the US carried on putting EBV and other herpes viruses at the centre of much of the research and discussion of CFS a lot is known and that is why this seems like a well worn track.

Ultimately, ME is a disease which is intitiated by a complex interplay of factors. Personally, I became ill after an enteroviral infection and I think they are heavily involved but even there the likes of polio was a mild transient disease in most people with only a few going on to have serious complications and we don't know what made the difference.
 
Pondering said:
EBV is epstein-barr not herpes. I am not sure I understand what you are saying? Why is it more likely that the underlying core is causing increased activity than the reverse? I am seriously curious.
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As others have stated EBV, CMV, HHV, VSV, HSV, etc are all the family of herpes viruses.

The current preponderance of evidence on ME/CFS indicates that it's much more likely that the underlying disease pathology is allowing these ubiquitous viruses to reactivate more often than in healthy people, but that there isn't any root connection or root cause and effect from these viruses. Whatever dysfunctional and chronic inflammatory/immune activation/metabolic process happening in ME/CFS cells just happens to give out the right stress signals and environment that causes reactivation.

Why did many of us, myself included, who took high dosages of Valcyte + Famvir or Valtrex daily for years get absolutely no improvement in my symptoms, disease process, or help with my decline. Nothing. If this were herpes viruses I would've seen at least some improvement and so would've the majority of others.
 
leokitten said:
Why did many of us, myself included, who took high dosages of Valcyte + Famvir or Valtrex daily for years get absolutely no improvement in my symptoms, disease process, or help with my decline. Nothing. If this were herpes viruses I would've seen at least some improvement and so would've the majority of others.
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Sometimes it's best to leave the immune system alone and not go off on pet theories. I didn't experience re-activating herpes viruses for the first 11 years of illness until I took immune modulators that caused a terrible relapse and messed up everything. Since then I get re-activations every 2 or so years.
 
Trying to figure out the significance of these findings.

Basically the paper shows that a lot of people have been exposed to CMV, HHV6 and EBV in the past, and there was no difference between patients and controls.

But they did find significantly more patients had active EBV infection. This was interpreted as reactivation rather than a primary EBV. Yet symptom profiles did not differ between patients with and without active EBV reactivation.

As far as I can see that doesn't tell us anything about EBV's role in causing or perpetuating ME. It does tell us that ME patients in this study were more susceptible to EBV reactivation but it doesn't tell us why (could be just another consequence of having ME?) - so what is the significance of the reactivations, especially since they don't make any difference to symptoms?

That's assuming the finding based on 58 Fukuda patients is actually solid.

Probably a dumb question but asking anyway: When they looked for viral DNA they found it in most participants' PBMCs (same for patients and controls) but they only found it in some patients' plasma (and almost none in controls). So why is there so much viral DNA in the PBMCs but so little in the plasma?
 
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