Salivary DNA loads for human herpes viruses 6 and 7 are correlated with disease phenotype in ME/CFS (Lee et al. 2021)

Pyrrhus

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

EDIT Aug 2021:
now published: https://www.frontiersin.org/articles/10.3389/fmed.2021.656692/full

Excerpt:
Lee et al 2021 said:
Myalgic Encephalomyelitis/ Chronic Fatigue Syndrome (ME/CFS) is a complex chronic condition affecting multiple body systems, with unknown cause, unclear pathogenesis mechanisms, and fluctuating symptoms which may lead to severe debilitation. It is frequently reported to have been triggered by an infection, particularly with herpes virus family members; however, there are no clear differences in exposure to, or seroprevalence of, any herpes virus in people with ME/CFS and healthy individuals. Herpes viruses exist in lytic and latent forms, and it is possible that ME/CFS is associated with viral reactivation, which has not been detectable previously due to insensitive testing methods.

Saliva samples were collected from 30 people living with ME/CFS at monthly intervals for six months and at times when they experienced symptom exacerbation, as well as from 14 healthy control individuals. The viral DNA load of the nine human herpes viruses was determined by digital droplet PCR. Symptoms were assessed by questionnaire at each time point.

Human herpes virus (HHV) 6B, HHV-7, herpes simplex virus 1 and Epstein Barr virus were detectable within the saliva samples, with higher HHV-6B and HHV-7 viral loads detected in people with ME/CFS than in healthy controls. Participants with ME/CFS could be broadly separated into two groups: one group displayed fluctuating patterns of herpes viruses detectable across the six months while the second group displayed more stable viral presentation. In the first group, there was positive correlation between HHV-6B and HHV-7 viral load and severity of symptom scores, including pain, neurocognition and autonomic dysfunction.

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.
 
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xebex

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just by chance i ended up getting a blood test whilst in a crash that showed active CMV infection. I do believe crashes cause the viruses to reactivate, now whether the overexertion causes the damaged immune system to allows the virus to reactivate or the virus is what causes the crash in the first place is yet to be seen. My personal opinion is that the immune system is faulty and the over exertion causes underlying viruses to reactivate.
 

Pyrrhus

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I do believe crashes cause the viruses to reactivate, now whether the overexertion causes the damaged immune system to allows the virus to reactivate or the virus is what causes the crash in the first place is yet to be seen.
I could see it either way:
  • Herpesviruses have a complicated logic built into their genetics that is constantly surveying the cellular status to "decide" whether to reactivate. One example of this is the reactivation of herpesviruses in response to pro-inflammatory cytokines.[1] If a crash leads to cellular conditions favorable to the herpesvirus, then the crash could lead to reactivation of a herpesvirus.
or
  • Exertion is often accompanied by activation of the sympathetic nervous system. Activation of the sympathetic nervous system decreases the function of NK cells.[2][3] NK cells are the most potent immune cell for preventing reactivation of herpesviruses, for some reason.[3][4] So activation of the sympathetic nervous system by exertion might lead to reactivation of a herpesvirus, which might lead to the symptoms of a crash. One example of this is the outbreak of cold sores that some people experience in response to stressful episodes.
References:
[1] https://pubmed.ncbi.nlm.nih.gov/9475116/
[2] https://content.iospress.com/download/advances-in-neuroimmune-biology/nib006?id=advances-in-neuroimmune-biology/nib006
[3] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7144531/
[4] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6788305/
 
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Pyrrhus

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I just realized that they did not exclude nuclear/genomic DNA when they did their PCR, so their study looked at all infected cells, whether they contained a latent infection or a reactivated infection.

However, given the fact that saliva generally contains short-lived cells, the presence of viral DNA probably represents active viral replication.

Lee et al 2021 said:
DNA was extracted from stored plasma samples using the QIAamp MinElute Virus Spin Kit (Qiagen), and from PBMC and saliva using the QIAamp DNA Mini Kit (Qiagen), according to the manufacturer’s instructions. Each DNA extraction run included a seronegative control sample and a Clinical Virology Multiplex I (National Institute for Biological Standards and Control (NIBSC)) positive extraction control: this comprised Adenovirus serotype 2, BK virus, CMV, EBV, HSV-1, HSV-2, HHV-6A, HHV-6B, JC virus, Parvo B19 virus and VZV.
 
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Wishful

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Is it the chicken or the egg?
Definitely the egg. If you consider one mutation or genetic pattern to be the dividing line between 'almost chicken' and 'chicken', the change had to occur between two 'almost chicken' DNA molecules that spliced together in the egg. Hmmm, no, the change could have occurred in the egg DNA grown in the 'almost chicken', so the question is still open.

A question appropriate for Easter. :)
 

Pyrrhus

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the change had to occur between two 'almost chicken' DNA molecules that spliced together in the egg.
...You may mean two "almost chicken" DNA chromosomes in the "almost chicken" sperm or the "almost chicken" unfertilized egg.

Then, when the "newly chicken" sperm met the "almost chicken" unfertilized egg, or when the "almost chicken" sperm met the "newly chicken" unfertilized egg...

Ok, now I give up.
 

Wishful

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The change from 'almost chicken' to 'true chicken' could have occurred in either parent or when the two DNA molecules combined. The mommy chicken wouldn't be able to tell the difference. Of course, the hen could have hatched a T-rex and probably not noticed anything unusual; they're not the smartest birds around.
 

Marylib

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@Pyrrhus - Did you see that the article is reviewed and published now? I can't seem to post it. Prusty reveiwed it, along with someone from NOVA Southeastern University. I wonder if this is one of the embargoed ones from the Invest in ME virtual conference last May. They think disease severity is correlating with HHV-6 and HHV-7 reactivation - among the herpes viruses. @Learner1 I think you were interested in this one too? Hopefully people have marked this thread as one to watch if they are interested.

https://www.frontiersin.org/articles/10.3389/fmed.2021.656692/full
 
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Pyrrhus

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@Pyrrhus - Did you see that the article is reviewed and published now? I can't seem to post it. Prusty reveiwed it, along with someone from NOVA Southeastern University. I wonder if this is one of the embargoed ones from the Invest in ME virtual conference last May. They think disease severity is correlating with HHV-6 and HHV-7 reactivation - among the herpes viruses. @Learner1 I think you were interested in this one too? Hopefully people have marked this thread as one to watch if they are interested.

https://www.frontiersin.org/articles/10.3389/fmed.2021.656692/full
Thanks for letting us know!

I have updated the link in the original post.
 

Violeta

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You probably know about this, but I'll just put it here in case someone hasn't seen it yet.

Herpes simplex virus type 1 infection activates the Epstein-Barr virus replicative cycle via a CREB-dependent mechanism


https://pubmed.ncbi.nlm.nih.gov/22188237/
I don't have a citation to prove what I'm thinking, so this is just a theory at this point, but does herpes virus activation of Epstein Barr virus have anything to do with the vagus nerve?
 
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ruben

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There was something on BBC this evening about autism and the big differences there are between different people who have an autism diagnosis. It said they were evaluating the saliva of many of these autistic people to see what studying saliva might reveal regarding the severity of their condition. Could this be relevant to ME/CFS?