Active Epstein-Barr Infections Found in Large ME/CFS Study

sometexan84

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This is my journey into CFS, I believe....

Enterovirus >> exercise + corticosteroid shots = Chronic enterovirus presence

Now major Th2 dominance – Temporary Immunodeficiency from unbalance

EBV reactivation from reduced Th1 (cellular immunity), and from reduced Immune surveillance.

EBV reactivation causes damage to immune system

EBV creates mitochondria dysfunction. This reduces energy production.

It also causes Cellular Hypothyroidism, which inhibits T3 transportation to cellular tissue (due to not enough mitochondria energy)

Mitochondria dysfunction can lead to our bodies going into a hypermetabolic state, constantly trying to get energy. If mitochondria isn’t working, then we can’t get energy from glucose or fatty acid. So then It has to break down our protein and muscle.

Hypermetabolic state leads to autonomic dysfunction. High heart rate, high sympathetic activity, fatigue, insomnia, etc.
 

ljimbo423

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Using both serological tests and PCR, this study provided a robust finding of an active EBV infection in about 20% of the ME/CFS patients tested. The authors asserted that this finding indicated “EBV is an important factor for the development of the disease” in at least a subset of patients.

If this finding is true and I'm not sure that it is. There are other studies that have found no evidence of EBV reactivation, above that of healthy controls. In fact Ron Davis found more viral reactivations in healthy controls than ME/CFS patients.

I don't see how the author of this paper can conclude that EBV is "an important factor for the development of the disease" and not a consequence of ME/CFS. To me that seems like a big leap, without evidence to support it.

Given that many healthy controls have these high viral titers and positive PCR tests and no symptoms, how can they conclude that the high viral titers and positive PCR tests for EBV are even causing symptoms in ME/CFS?

I don't think they can. It's a hypothesis they have come up with, no more no less. As I said, this might be an accurate finding or not. Even if it is, there's no evidence that EBV is causing the ME/CFS patients disease or symptoms.

This study shows a possible correlation of EBV to ME/CFS. Not a causation of symptoms.

They will need to go a lot further to show EBV in ME/CFS as a cause of symptoms.
 

Wishful

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The paper says: "ME/CFS also produces symptoms similar to those produced by “sickness behavior”: a process initiated by the brain that’s designed to keep us in bed to stop spreading an infection."

Well, for one thing it wasn't "designed", it was the result of evolution, meaning that the behaviour allowed animals to propagate longer. I was going to argue that the purpose was to place the body into a state where its resources could go towards fighting the infection better, but on second thought, preventing the spread of the infection might be a driver for evolution, but if that was the driver, I think it would act differently, encouraging the victim to actively avoid others of its species. Do no animals with sickness behaviour curl up in their den with other members around? If avoidance of spreading the infection is the goal, it should trigger fear of its own species, or the desire to roam, or some such behaviour. I still think self-preservation is the goal, rather than reducing the spread of infection.

I agree with ljimbo423 that the study is too weak to support its conclusions. A correlation with ME in some PWME seems reasonable, but it certainly doesn't convince me that it's the cause of ME in everyone.
 

Treeman

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but it certainly doesn't convince me that it's the cause of ME in everyone.
They said, "Using both serological tests and PCR, this study provided a robust finding of an active EBV infection in about 20% of the ME/CFS patients tested. The authors asserted that this finding indicated “EBV is an important factor for the development of the disease” in at least a subset of patients."
 

ljimbo423

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The authors asserted that this finding indicated “EBV is an important factor for the development of the disease” in at least a subset of patients."
This is what I don't understand. How do they come to the conclusion that EBV is causing symptoms in 20% of ME/CFS patients? High EBV titers or DNA found in the blood by PCR, does not mean EBV is causing symptoms.

There are other studies that show active EBV in healthy controls, both through PCR testing and antibody testing. Yet healthy controls do not have symptoms of ME/CFS or EBV.

It just seems to me that they are making a connection to it causing symptoms without evidence.
 
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If avoidance of spreading the infection is the goal, it should trigger fear of its own species, or the desire to roam, or some such behaviour.
Using your argument, it seems like triggering fear, or go out roaming...or be very socially distant- those conditions are NOT very conducive to feeling better or healing from injury or infection.

We may need help when sick or injured. Somebody to bring supplies, keep the fire going.

Thinking about the term- Sickness Behavior...seems a bit of a misnomer, in that Behaviors could be viewed as activities that are under our direct control. You can decide to: behave.

Maybe a better term would be, like Sickness Response.
 

Wishful

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The authors asserted that this finding indicated “EBV is an important factor for the development of the disease” in at least a subset of patients."
Well, yes, if the 'subset of patients' is defined as those for whom EBV is an important factor, then it's a self-defined truth. I don't think the study determined whether it's a cause or an effect of the development of the disease. I suppose they can test that by finding patients who had suitable viral tests done before developing ME. They could also measure viral and antibody levels frequently in patients whose symptom severity fluctuates a lot and see whether there's a correlation and which happens first.
 

Wishful

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Using your argument, it seems like triggering fear, or go out roaming...or be very socially distant- those conditions are NOT very conducive to feeling better or healing from injury or infection.
Yes, it would be sacrificing the individual for the protection of the group. If protecting the group from the spread of infection was the goal, then you'd see infected individuals running off to most likely die. That might spread the infection to a distant group, but that would be okay, since your family's genes would continue, and might even benefit from you killing off families in other territories (fresh territory for your family's young to spread to!). Since it doesn't work that way, self-survival seems like a more likely goal.


Sickness Behavior...seems a bit of a misnomer, in that Behaviors could be viewed as activities that are under our direct control.
No, the definition doesn't require direct control; it's just the outcome. Murderous behaviour might be direct choice, or it might be due to brain damage or chemical alteration of neural pathways or hormone activity. Non-sentient systems can have behaviours. Even bacteria have behaviours. I don't have a problem with the term "sickness behaviour".
 

Treeman

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This is what I don't understand. How do they come to the conclusion that EBV is causing symptoms in 20% of ME/CFS patients? High EBV titers or DNA found in the blood by PCR, does not mean EBV is causing symptoms.

There are other studies that show active EBV in healthy controls, both through PCR testing and antibody testing. Yet healthy controls do not have symptoms of ME/CFS or EBV.

It just seems to me that they are making a connection to it causing symptoms without evidence.
I think the use of the word
is just a suggestion rather then a definitive.
 
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The paper says: "ME/CFS also produces symptoms similar to those produced by “sickness behavior”: a process initiated by the brain that’s designed to keep us in bed to stop spreading an infection."
I think you will find that this does not come from the paper, its what Cort Johnson says. As to the research...I would like to say it's useful, but it gets a thumbs down from me. Pretty much the same old stuff.
 

ljimbo423

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This is the actual abstract of the study-

Cytomegalovirus, Epstein-Barr virus, and human herpesvirus-6 infections in patients with myalgic еncephalomyelitis/chronic fatigue syndrome
Evelina Shikova 1 2, Valentina Reshkova 3, Аntoniya Kumanova 1, Sevdalina Raleva 1, Dora Alexandrova 2, Natasa Capo 4 5, Modra Murovska 6, European Network on ME/CFS (EUROMENE)
Affiliations expand
Full-text linksCite
Abstract
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 patients with ME/CFS and 50 healthy controls. Virus-specific antibodies were detected by enzyme-linked immunosorbent assay and viral genomic sequences in peripheral blood mononuclear cell (PBMCs) and plasma samples by nested polymerase chain reaction (PCR).

We did not observe any significant differences in virus-specific immunoglobulin G and immunoglobulin M positivity rates between patients with ME/CFS 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%, and 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 = .0027).

No ME/CFS and control individuals with active CMV and HHV-6 infection were observed.

In conclusion, this study using both serological and PCR-based techniques for distinguishing between active and latent infection showed high rate of active EBV infection among patients with ME/CFS indicating that at least in a subset of cases, EBV is important factor for the development of disease.
My bolding of sentences.

https://pubmed.ncbi.nlm.nih.gov/32129496/
 

Hip

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Sometimes I get the impression these studies are more a test of the viral detection methods used, than they are a test of ME/CFS patients.

This study found no difference between ME/CFS patients and controls with respect to herpesvirus antibody levels, but a 2012 study found that 94% of ME/CFS patients were positive on the EBV early antigen diffuse test, versus 32% of controls.
 

ljimbo423

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This study found no difference between ME/CFS patients and controls with respect to herpesvirus antibody levels, but a 2012 study found that 94% of ME/CFS patients were positive on the EBV early antigen diffuse test, versus 32% of controls.
94% seems like an incredibly high number. Has this study ever been duplicated? In order for these findings to be credible, there would need to be multiple studies showing this same high percentage of EBV (EA) in patients.

As I pointed out above. Even if these numbers were correct and I don't think they are. That doesn't show that the patients ME/CFS symptoms are being caused by an EBV reactivation.

Many healthy controls have EBV re-activations and no symptoms of ME/CFS or EBV. As shown in the study you posted. 32% of healthy controls were also positive for EBV (EA). As healthy controls they would not have symptoms of EBV or ME/CFS.
 

sometexan84

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Indeed.

I've been on Valacyclovir for 2 1/2 months now. It should be another 3 months-ish before I know if it's working. But I did have a Herx-like reaction 5-6 wks into taking it, which is a good sign that it is working.

Started on Azithromycin (Zithromax) 6 days ago, for Chlamydia pneumoniae and Streptococcus infections. This is just a 1 or 2 month treatment. Today I actually feel abnormally weak and tired. I think it's either Herx-like reaction from the Azithromycin or from the Magnesium Malate supplement I just started on.