Salivary DNA loads for human herpes viruses 6 and 7 are correlated with disease phenotype in ME/CFS, Lee, Lacerda, Nacul, Cliff et al, preprint 2021

Full title:
Salivary DNA loads for human herpes viruses 6 and 7 are correlated with disease phenotype in Myalgic Encephalomyelitis/ Chronic Fatigue Syndrome

https://www.medrxiv.org/content/10.1101/2021.01.06.20248486v1

 

I think it is a consequence of dysregulated immune function for a subset that would include me.

 

Canadian and/or Fukuda selection criteria. Would be nice if they would give Fukuda up.

Why would it necessarily be one or the other? Reduced available energy (due to ME) for the immune system might allow for herpes reactivation, which then causes issues as the immune system uses more energy trying to control it, seems to be a logical possibility to me.

 

Very interesting but again an association is a long way from indicating cause and effect in either direction. As @Andy points out both phenomena could be arising from a distinct common cause.

Are there similar fluctuations in viral loads in other conditions?

 

My ME didn't start out with viral reactivations, I actually felt "virus-free" for 11 years. Something changed along the way where I'm feeling 'viral' 80% of the time. Some are actual viruses but others not so much. I'm not going to my GP every month to find out.

 

My guess is that they'd find a similar correlation with most viral infections. I think that anything that influences the immune system(s) will have an effect on ME symptom severity.

 

Interesting.
One teenager we know was treated with antivirals for HHV 6 and is now mildly affected.
Could be coincidence of course .....

 

This would be the typical progress of latent and reactivating infections. I think the authors try to clarify that the association doesn't imply causality and that HHVs are necessarily the primary target of treatment. Just because you get HSV during PEM, it doesn't mean that HSV treatment could provide any benefit. Maybe, it is a whole group of viruses that share a certain genome. The more of them you get infected with, the greater the influence on the immune system of people with certain genotypes (TBD), the greater the overall lysis/reactivation dynamic of latent co-infected virus reservoirs.

Theoretically, EBV could also play a part. Saliva samples don't indicate if lysis happens locally and contained in the lymphatic system. I think long-term studies with children could clarify which viruses initially trigger CFS, to narrow down potential commonalities and genomes. HHVs, EBV, and CMV are all known to dysregulate immune function in the long term.

I don't know any antiviral that works with the whole range of viruses. But maybe there is an antiviral that is specific to their common genomes. Regardless, virustatics might only suppress the lysis, which might influence PEM susceptibility, but altered lymphocytes would not return to their normal state because of this. This means virustatics would have to be taken continuously. The overall outcome might be similar to what has been observed for treatment-resistant Lyme Borreliosis, which is also dependant on the human HLA genotype. Initially, antibiotic therapy can help for Lyme Borreliosis, but long-term outcomes of therapy are not promising. It might work, but there are also anecdotes of it becoming worse. Maybe (true) antibiotic resistances are involved then, I don't know. The HLA type predisposes patients by general susceptibility, not antibiotic-specifically (10.1006/jaut.2000.0495).

 

So they're just replicating citation 36.

They reference citation 36 as "herpesvirus are found in saliva in CFS patients"

But it's more than that: "Human herpesvirus 6 and 7 are biomarkers for fatigue, which distinguish between physiological fatigue and pathological fatigue."

Why wouldn't sicker patients have a higher viral load? That's uniform throughout almost every illness, dermatomyositis, MS, Stevens Johnson syndrome, asthma, obstructive sleep apnea, depression.

What's your hypothesis? Why are you doing the study?

 

I assume the study samples they're using from the biobank were already selected/collected using these criteria.

 

True, but I know they still look to use it in studies and they still list it as inclusion criteria for Biobank samples.

 

Only glanced at this but it reminds me of Bupesh Prusty's hypothesis i.e. ME is related to the effects of latent herpesvirus.

Extract from paper:
"The results indicate that fluctuating viral load, related to herpesvirus reactivation state, may play a role in ME/CFS pathogenesis, or might be a consequence of dysregulated immune function. The sampling strategy and molecular tools developed permit large-scale epidemiological investigations."