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The Epstein-Barr Virus – Could it be Causing Neuroinflammation in ME/CFS?

EBV has been a virus of interest since almost day one in chronic fatigue syndrome (ME/CFS). In fact, at one point, EBV was such a hot topic that ME/CFS was called for a time “chronic Epstein-Barr virus” disease.

Virion EBV

Epstein-Barr virus virions (circular centers). Virions are the form of the virus which infects other cells. EBV dUTPase is released when the process of creating virions is aborted…

While studies have generally failed to find evidence of EBV reactivation, EBV has never fallen out of the picture with ME/CFS and for good reason. For one, it’s entirely possible that researchers were looking in the wrong place to determine if EBV is an issue in this disease.  For another, EBV infection in adolescence or later and the infectious mononucleosis (glandular fever) it produces, is a common trigger in ME/CFS, and is a proven risk factor for multiple sclerosis.

Besides ME/CFS, researchers are continuing to assess the role EBV may play in many serious illnesses including multiple sclerosis (MS), systemic lupus erythematosus (SLE), Guillain-Barre Syndrome, several cancers,  rheumatoid arthritis (RA), juvenile idiopathic arthritis (JIA), inflammatory bowel disease (IBD), celiac disease, schizophrenia, and others.

Neuroinflammation, of course, is a hot, hot (pun intended) topic in both ME/CFS and fibromyalgia. Recent studies suggest neuroinflammation is present in both diseases and major studies are underway to validate that finding.

Nobody until now, though has attempted to complete the circle, and bring that “original gangster” in ME/CFS – Epstein Barr Virus – and the new guy in town – neuroinflammation – together.  Could EBV be causing or contributing to the neuroinflammation present in the disease?

Some History

Over 10 years of work by an Ohio State University team lead by Maria Ariza and Marshall Williams has been turning the EBV question in ME/CFS on its head. High levels of EBV, they believe, are not the problem in ME/CFS at all. In fact, their studies suggest that EBV may be at its most dangerous in ME/CFS not when it reactivates – but when it fails to reactivate properly.

dTUPase model

The Ohio State University dUTPase continuing NIH grant is in its 9th year.

By the time the impaired immune systems of people with ME/CFS have started knocking down EBV’s attempt at reactivation, the bug has already produced a potentially pathogenic protein called dUTPase. The Ohio State University researchers believe this protein may be wreaking havoc in a large subset of people with ME/CFS.

With the NIH supporting them every step of the way – their continuing grant on dUTPase is now in its 9th year – the evidence that this protein is contributing to ME/CFS (and other diseases) has continued to build.

In 2012, the group found evidence that the immune systems of people in a large subset of ME/CFS patients were indeed battling this protein. Just a year later they showed that even when viral loads of EBV were low, dUTPase could still be triggering a significant pro-inflammatory response. That finding suggested that failed prior attempts to link EBV reactivation to ME/CFS were barking up the wrong tree.

Two years later, they demonstrated that dUTPase was able to make its way into exosomes (now a major topic of interest in ME/CFS), cross the blood-brain barrier, produce major immune effects, and perhaps even promote further EBV infections.

Then a 2017 study added another herpesvirus long suspected in ME/CFS – HHV-6 – to the mix. That study found antibodies to dUTPases produced by both EBV and HHV-6 in almost fifty percent of the ME/CFS patients.  That suggested that the two herpesviruses might even be reactivating each other – a feature found in some very immune suppressed states including organ transplant patients and drug induced hypersensitivity syndrome.

Then again, really significant immune suppression in ME/CFS may not be a surprise. Up to 75% of ME/CFS patients were found to have low numbers of the B-cells designed to keep EBV in check in a recent study.

If the immune system wasn’t having enough trouble, in 2017 the first evidence of an autoimmune process involving EBV dUTPase was found in ME/CFS. Autoantibodies to the human dUTPases (humans produce a dUTPase as well) were found in ME/CFS – at much higher levels than in healthy controls (39% vs. 5%). That suggested that the immune response to EBV and HHV-6 dUTPase may have gone awry in some people with ME/CFS. Their bodies were now attacking their own human dUTPase.

The 2019 Study

In the present study we provide further evidence…. (that) dUTPase protein…could contribute to the development of a neuroinflammatory microenvironment in the brain(s) (of a subset of ME/CFS patients.)  The authors

Epstein-Barr Virus dUTPase Induces Neuroinflammatory Mediators: Implications for Myalgic Encephalomyelitis/Chronic Fatigue Syndrome. Marshall V. Williams PhD; Brandon Cox ; William P. Lafuse PhD; and Maria Eugenia Ariza, PhD. Clinical Therapeutics March 2019

In 2019, the team took another step. In an earlier study they’d demonstrated that the EBV dUTPase protein could be causing or contributing to the symptoms present in ME/CFS. Since many of these symptoms can be produced by the brain, they next asked if the enzyme could be affecting the integrity of the blood-brain barrier (BBB) and other aspects of neuroinflammation.

There’s a pretty good reason to believe this might be the case. EBV, after all, has been associated with some pretty nasty neurological diseases. The virus loves to hang out in nerve cells and astrocytes, is a risk factor for M.S. and has, in fact, been found scattered throughout the astrocytes and microglial cells in MS patients’ brains.

The Ohio State University researchers plopped the dUTPase protein into a variety of cells and then determined how it affected the expression of genes that play an important role in maintaining the blood brain barrier (BBB) and the functioning of various brain cells (cerebral microvascular endothelial cells, astrocytes, microglia cells).

The big bug’s dUTPase protein turned out to be quite adept at tweaking genes and proteins associated with the BBB and neuroinflammation. It turned on 12 of 15 genes and 32 of the 100 proteins examined in vitro (in the lab) and 34 of the 84 genes examined in mice.

The fact that these genes play a role in BBB integrity/function, fatigue, pain synapses and their functioning as well as tryptophan, dopamine, and serotonin metabolism suggested that this enzyme, in or out of the brain, could conceivably cause widespread problems.

How the Blood-Brain Barrier Works

 

 

All in all, the protein appeared to be doing its best to find a way to get EBV into the brain. That’s perhaps not a surprise given how much EBV loves to hang out in neurons. As EBV dUTPase was down regulating the expression of genes dedicated to producing a tight BBB it was “strongly” inducing the expression of two cytokines (IL-6 and IL-1β) known to disrupt The BBB.

If EBV dUTPase gets inside the brain, it seems almost guaranteed to cause neuroinflammation.  Studies indicate it can trigger microglial cells and astrocytes (star-shaped immune cells in the brain) to produce potent pro-inflammatory cytokines (IL-6, IL-1β and TNF-α). It also prompts astrocytes to produce a substance (PTGS2/COX-2) associated with neuroninflammatory toxicity. Plus it’s able to alter the expression of genes associated with pain (GPR8451 and GCH152) and fatigue (TBC1D153) to boot.

In mice, it altered the expression of genes associated with cognition (synaptic plasticity, learning and memory).  One of the more intriguing findings, given the possible disruption of the kynurenine pathway in ME/CFS, was the protein’s potential to increase synthesis of a potent neurotoxin called quinolinic acid. Genes associated with the metabolism of two of the major neurotransmitters in the brain, dopamine, and serotonin, were also affected.

EBV dUTPase neuroinflammation

If EBV dUTPase has indeed been able to get into ME/CFS patient’s brains it seems almost guaranteed to cause neuroinflammation

All in all, EBV dUTPase is not a protein anyone wants hanging out in their head. It is, however, a protein that could potentially produce a lot of the problems found in ME/CFS.  This study demonstrated that the protein appears to have the capability to make its way to ME/CFS patient’s brains. Determining if it has will take further investigations, however.

It should be noted that the protein and its antibodies (or the autoantibodies to the human dUTPase) are not found in everyone with ME/CFS but the potential subset – ranging from 30% to 60% of those tested so far, is pretty darn large.

Plus, the virus is heavily implicated in the stress response. If you feel like your nervous system is over-reacting to, well, anything (or everything), EBV and this protein could be a factor. Of all the viruses, EBV and the herpesviruses love most to come out and play when one’s system is stressed.

In fact, Ron Glaser, one of the initiators of the EBV dUTPase research effort, demonstrated back in 1991 that EBV thrives in situations of psychological stress. Given the enormous stress people with ME/CFS are under, and the affects the illness has on both axes of the stress response, it makes sense that the virus might be continually trying to reactivate – and spilling it’s toxic protein into the bloodstreams of some people with this disease.

A Good-bye to a Pioneer

Ron Glaser

Glaser was shocked he couldn’t get his ME/CFS grant applications funded at the NIH

Ron Glaser was something of a legend in his own time. With his doctorate in pathology, his EBV citations alone total over 100. All told he published over 300 papers. Glaser co-founded Institute for Behavioral Medicine Research, which under his leadership brought in over 140 million in grant money over 20 years. At one point he was one of the world’s most cited authors.

His memorials mention his impact on the psychoneuroimmunological (PNI) field, his enthusiasm, (and the red and white Corvette he loved). What they don’t mention is that this leader also devoted time to a much neglected field called chronic fatigue syndrome. Glaser, in fact, took the time out of his busy schedule to sit on the now disbanded federal advisory committee for ME/CFS (CFSAC).

I vividly remember talking to him. He was not a man to mince words. An accomplished researcher with a long history of grant success, Glaser was first shocked, and then very angry at the rejections piling up for his ME/CFS grant applications. He just couldn’t understand it. Never in his decades of work had he experienced such a thing.

Stating, ironically, he couldn’t stand the stress (he did look like he was about to burst a blood vessel), he eventually moved on, but not before making his experiences perfectly clear to the federal advisory committee and everyone around him.

Glaser was not happy at not being able to work more in ME/CFS, but the work he did did not go for naught. Glaser first published on EBV dUTPase in 1985 and on EBV and ME/CFS in 1988 and his work lives on in Ariza and William’s studies on ME/CFS today. Check out a memorium to Ron here. 

Marshall Williams – On the Continuing Hunt for EBV dUTPase in ME/CFS

What about the connection between this protein and the presence of infectious mononucleosis/glandular fever in ME/CFS? Do we have any idea if the enzyme is more likely to be found in people who’s disease was triggered by IM or who had an acute, flu-like onset?

That is an excellent question. We are in the process of trying to obtain longitudinal serum samples from an IM cohort who developed CFS as well as age matched patients who had IM but never developed CFS. Hopefully, that may address this question.

EBV dUTPase exosomes

When EBV (lytic) replication is aborted it tosses EBV dUTPase into exosomes (circles with red marks) which, after binding to TLR receptors on immune cells, tells those cells to turn on proinflammatory and other genes (from Ariza, Williams and Glazer -https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0069827)

This study demonstrated that this enzyme has the potential to disrupt the BBB and enter the brain – and as added bonus – perhaps helps get EBV into the brain. Is there any way to tell if this has actually happened in ME/CFS?

Not really at this point but maybe in the future. Screening CSF from ME/CFS patients for antibodies to the EBV-dUTPase or HHV-6 dUTPase might suggest potentially the presence of these viruses in the brain.

Exosome research is heating up in ME/CFS. Some anecdotal reports show that exosomes in the blood may be affecting energy metabolism and other functions. Could herpesvirus dUTPases be involved? Is there any more information on exosomes and EBV dUTPases?

We have not looked at energy metabolism but there are some reports in the literature that some herpesviruses including EBV and HHV-6 alter mitochondrial function. There is information concerning EBV products in exosomes but most of these have focused on proteins/microRNAs involved with latency.

What is next for your team? 

We are in the process of submitting a manuscript detailing a mechanism(s) by which the EBV-dUTPase and to a lesser extent the HHV-6 dUTPase alter germinal center function, which could contribute to autoimmunity in CFS patients. We will be continuing these studies as well as those regarding neuroinflammation. (B-cells manufacture autoantibodies in the germinal centers found in the lymph nodes and spleen)

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29 Comments

  • Kate

    July 4, 2019 at 1:35 am - Reply

    This is closely related to what Dr Davis presented recently. I sure hope they are all talking to each other. Do we think then that we all have completely different conditions causing the same symptoms? Some people have cervical instability or other spinal mechanical problems, some have bad proteins, some are in a metabolic trap, some have autoimmune problems, some are in a toxic sepsis state, some are in a dauer state, etc etc….or do we think it’s all related somehow? And Cort, neuroinfkammation is hardly the new guy. They reached that conclusion when the WHO named it myalgic encephalomyelitis 80 years ago.

    • Cort Johnson

      July 4, 2019 at 12:53 pm - Reply

      It’s a great question. My guess is that there are a number of ways to produce the same result (neuroinflammation) in ME/CFS and entirely different forms are present as well. I sure hope there’s a core commonality.

      It’s true that myalgic encephalomyelitis does refer to inflammation of the spinal cord/brain (the term was coined, I believe, though, by Acheson in 1959), the research after that did not indicate that neuroinflammation was present because the tools used back then were not strong enough to detect the milder form of neuroinflammation recent studies have shown in ME/CFS. Instead “white matter hyperintensities” were found but they were found in different areas of the brain in different people with ME/CFS; i.e. they were not diagnostic.

  • Learner1

    July 4, 2019 at 1:45 pm - Reply

    Thank you, Cort! This is very important to know – nice to have all this tied together!

    As always, I’m impatient, and wanting to translate this into something usable to help us improve now, even before all the work is complete and papers published which will likely take another 5 years or more. Questions popping into my head:

    – Beyond the duTPase antibody tests, what would all the other EBV lab tests look like if this were going on?

    – Any other cytokines raised besides IL-6 and IL-1B?

    – Would valganciclovir or valacyclovir affect/improve symptoms, reduce the quantity, rid the body of EBV (and HHV6) viral material? Would anything else, like artesunate, oxygen, etc.?

    – What else could one take to reduce neuroinflammation?

    – How exactly does this impact the immune system?

    – How does it affect the vagal nerve?

    – Could it also cause CCI?

    Thanks again!

  • Erik Johnson

    July 4, 2019 at 2:54 pm - Reply

    CFS was coined because Cheney & Peterson disproved CEBV Syndrome.
    Dr Cheney found EBV was neither the cause, nor was it necessary to even be present.

    It was the new “HBLV” now known as HHV6A that formed the foundation for what Dr Peterson calls “classic CFS”

    At the last Open Medicine Foundation I asked him if anything had changed since then.
    He said that nothing has.

  • Aidan

    July 4, 2019 at 3:40 pm - Reply

    I have now seen in ME/CFS Fibro EDS3 an entire Family all diagnosed with type VIII & IX of both types of GSD’s but under the newer criteria now they have 2 types of No.IX GSD’s combined

    Glycogen Storage Disease they classified VIII type as a IX I thing there are 3 types of IX GSD & I doubt EBV is involved at all…I have also seen types III, V & XIII GSD in patients with this

    illness as well misdiagnosed all along…I would not be surprised that HATS Hereditary Alpha Tryptasemia Syndrome is also involved, I do know now some also have the Alpha Gal Meat

    Allergy combined i ME/CFS Fibro or EDS 3…I doubt also Virus or Bacteria were ever involved unless you had Alpha Gal you need 10 days of antibiotics & diet…Also make sure one does

    not have Genetic (HFI) Hereditary Fructose Intolerance as well I have seen Positives…

  • Betty Mekdeci

    July 4, 2019 at 3:52 pm - Reply

    I have been re-reading Hilliary Johnson’s tome on the Chronic Fatigue Syndrome Epidemic, “Osler’s Web” which follows the illness as it moved across the country starting in LA and San Francisco in 1980. While stress is part of life always, I find it unbelievable that each cluster of ME/CFS patients was a group of people with similar stress.

    A second point I have been thinking about is the use of Valtrex mainly for reactivated EBV. Valtrex is not used for mono which is of course an active infection with EBV. Why would you use it for a reactivation? Valtrex is not a drug of choice for HHV6.

    A third point is to recommend that readers of this site go to the HHV6 Foundation web site and look up the research going on at Baylor. A product called Viralym-M, in phase II trials, could be useful to treat a number of viruses found in ME/CFS patients. My understanding of the drug is that it works like a more sophisticated form of Transfer Factor.

    • Cort Johnson

      July 4, 2019 at 4:38 pm - Reply

      Eww..Thanks for the tip on new herpes drug. Looking forward to checking that out

      I agree about the stress! I was actually in the opposite of a stressful environment when I got ill – I had found my niche (ecology), was active physically and loving the forest environment I was at school in – then blasted ME/CFS showed up. I more think genetics or a powerful strain of EBV or bad luck must have played roles for many.

      Afterwards, though, my stress response has been on a knife’s edge. I don’t mean upset about having ME/CFS either. Something has turned it on all the time (for me). If EBV is a culprit I think it must either be kicking our stress response in the teeth or something else is. It makes sense EBV would do this since it thrives on stress!

      What is a better drug than Valtrex? Is Famvir better?

  • elvira

    July 4, 2019 at 7:01 pm - Reply

    Ottawa based Byron Hyde, Md (working exclusively with ME/CFS patients, was focusing on it for a very long time.

  • Flora

    July 4, 2019 at 8:40 pm - Reply

    36% of females with Endometriosis have a comorbid diagnosis of ME/CFS it’s hard to think of a more stressful “benign” condition than Endometriosis as it’s so painful and can impact so many organs in the pelvis and elsewhere.

  • naomi allen

    July 4, 2019 at 9:02 pm - Reply

    Wow! It just boggles my mind trying to read through all of this, barely able to keep up with following the printed conversation – i really hope my brain can work so well again some day (i have been ill 30+ years, and though not as severe as others, with rapidly declining physical abilities, and even faster on the cognitive scale, not knowing what to expect in the future is daunting. Thanks to all those carrying out the research, and especially to those who help make it understandable and hopeful for me.

  • kathryn

    July 4, 2019 at 10:07 pm - Reply

    A fellow patient told me that Montoya told her that one must use Valcyte for a year or two, and it forces the EBV out of the cells (B cells?) so that Valtrex can treat that, for another year or two.

  • Susan ridge

    July 4, 2019 at 10:57 pm - Reply

    It seems obvious to me that there are so many variables we will never find a single cause. All of the research points to neuroinflammation and metabolic disorders. Even if we find subsets there will always be someone who doesnt fit. I am managing my mecfs quite well and now able to work full time and swim and go to the gym every day. I found that i needed to have everything that was wrong in my body fixed before i could start to make a difference: coeliac disease, micoplasma fermentans, mercury toxicity, vitamin deficiencies, parasites, autoimmune dry eye – sjogrens, ebv, cmv, hypoglcemia, insulin resistance….plus many more. I had treatments for all of these and improved a bit. Then the road to rebuild and recover included understanding the role of cortisol and the adrenal axis. I made myself not react to any stress, and if something did stress me i took long slow deep breaths to calm it straight away. Even excitement about good stuff is bad….stay like a buddhist monk in meditation. Dietwise no gluten, dairy, sugar, caffeine, yeast, msg. Small regular meals high in protein low GI. Exercise is the hardest…finding your starting point…should be slow gentle nonaerobic with deep breathing. As you get better you can proceed to a bit of aerobic if you dont get symptoms….stay away from sick people…be happy all the time….it is hard but it may work for you. Good luck to us all

  • Barbara

    July 4, 2019 at 11:06 pm - Reply

    Dr. Peterson put me on Valtrex for a year. It had no impact on my EBV titres. Oddly, it benefited another symptom: neuro mediated hypertension: NMH. I was able to walk and stand instead of feeling faint.
    however, in one of the blood labs, it seems to have given rise to a problematic bunch of cells which I now have to monitor which did not exist previously

  • Kim Quintero

    July 5, 2019 at 12:43 am - Reply

    I’ve had Epstein Barr and mono, but never had CFS or ME. However I do have Fibromyalgia. So not sure if I agree with this. My brother is a scizephania, but he never had any viruses. I think more research and testing with individuals who have these viruses needs to be done. I sure would volunteer. L

  • Cort Johnson

    July 5, 2019 at 12:50 am - Reply

    Eric – Doctors don’t disprove things – researchers do. They’re certainly not testing for EBV dUTPase which has nothing to do with antibodies or other markers of EBV reactivation. It has to be emphasized that markers of viral load or immune activation (the EBV antibodies tested for) – which how EBV has almost always been assessed – have nothing to do with this research.

  • Cort Johnson

    July 5, 2019 at 12:52 am - Reply

    Aidan – I agree that it’s going to be very interesting to see how GSD plays out in ME/CFS…I’m sure it’s going to pop up more and more as researchers start to loo for it.

  • Donna

    July 5, 2019 at 8:56 am - Reply

    I think THIS is funny, “The Medical Medium “- Anthony William- (he has all those health books out.) Has said for yrs, that CFS is from the Epstein-Barr Virus and puts everyone on CELERY JUICE.

  • Sarah R.

    July 5, 2019 at 9:55 pm - Reply

    Thanks, Cort. As usual, an understandable review of gnarly research.

    • Cort Johnson

      July 6, 2019 at 3:31 pm - Reply

      Thanks!

  • Crystal

    July 6, 2019 at 12:23 am - Reply

    Interesting thing is that everytime I “kill” viruses, whether with pharmaceutical antivirals or “natural” ones such as lysine I have a SEVERE mental/depressive and I mean severe, that is very unusual for me , reaction. Like I can literally feel the neuroinflammation. I guess what I’m saying is I do the think that there is some viral connection, but I think that just “killing ” them is somehow not the exact answer.

  • dejurgen

    July 6, 2019 at 9:16 am - Reply

    Maybe “what bad does EBV do” is only part of the question. Maybe another part could be “what good can’t it do in ME patients?”.

    I know the last question is controversial for people suffering so much of this disease. But the evolution of EBV is so much interwoven with human evolution. Even now, 95% or so of adults has EBV in its body. That’s probably less then in the past and an increasing number of people only gets EBV later in life due to increased hygiene.

    Having such an “intimate” relationship with human evolution, EBV has an interest in keeping our health at a reasonable level. First of all it learned to help its own survival, but helping our survival is in its own interests too. Part of that can be seen in some EBV viral DNA that proved to be valuable enough to incorporate it in human DNA.

    I won’t go that far too call EBV something good, but it has to have at least a “fairly neutral” impact on our life quality and expectation. As it obviously has some bad properties, keeping its effects neutral requires some good properties to balance that out IMO. Then the questions are: what supposed good qualities has EBV? what supposed good qualities are less expressed in ME patients? what supposed good qualities are a poor match with other things going on in ME patients?

    For example some believe that retro viruses provide some “immunity training” to the human immune system. That should help distinct self from not-self or in other words help prevent auto immunity problems. Such supposed “training” would be better at a young age as auto immunity problems tend to grow over time. Part of how auto immunity develops is by transforming “unspecialized” immune cells into immune cells specialized in recognizing a certain (supposed) pathogen and increase the numbers of this type of specialized cells. The better the “training” at an early age, the less of those their should be IMO.

    Then their is another nasty part of EBV: it is a known opportunistic pathogen. It detects when one has a sort of acute problem and alters immune functioning (and reactivates at the same time). I could argue that spreading itself further in the body may not be the first goal of a reactivation: the virus already needs to be solidly in the body in order to be able to reactivate first. And a virus that wishes to survive in the body during the entire lifetime of that body must have learned to limit its own growth in order to not kill the host IMO. So the prime goal of reactivation seems to be able to make the host contagious and spreads the disease to other people. Doing so when the immune system is challenged may be smart: if the host is ill, then maybe the people around it are ill too. And that would ease their infection.

    If the prime goal is not to further infection in the host, then reactivation may not be that problematic in a healthy person. Maybe this could even be partly a symbiotic functioning with EBV “alerting” and triggering the human immune system to go into a higher level. If so, that would allow the immune system to tone down during “no problems” periods and only increase its strength during times of trouble. That would in fact *decrease* auto immune problems in healthy people and reduce the cost of the immune system to the body.

    Now if we combine these two ideas:
    * at young age, people who had not got EBV infected lack proper immune training recognizing self from invaders
    * that allows to set the initial seeds for a potential future auto immunity as some (small amount of) immune cells got specialized wrongfully in recognizing self as a target
    * that also allows some problems that should be tackled to remain under the radar for years (and grow / pile up) as the immune system didn’t get the proper training to recognize them as a real threat (or EBV didn’t set immune strength to its supposed “normal” value as there was no EBV).
    * when this person gets EBV as an adult, the immune system is improperly trained and at a “wrong” level causing the infection to be nastier then the “gentle” infection EBV learned to be at a young age.

    But most importantly: short after the infection when (it should be) going in its latency faze, EBV exerts its “symbiotic role” of alerting its host and point to a threat that has been pilling up in the host for years. That could be for example large deposits of coagulated prions (self replicating misfolded proteins causing a myriad of diseases) or a latent bacterial infection of the inner eye.

    These supposed underlying problems could be at such a stage that the immune system has far more effort to tackle it then when it would have done so at a young age. What would have been a small and near unnoticeable acute immune fight and pathogen cleanup when alerted to this problem (due to young age EBV infection exposing the problem to the immune system) now becomes a hard and long semi-chronic immune fight. That might be in fact the cause of EBV causing so much more intense disease (mono) at adult age compared to a younger age (much more problems that EBV alerts the immune system to have accumulated over time).

    Even when the initial supposed cleanup is done and the acute faze of the disease (mono) is over, the intense fight may have grown the seeds for auto immunity at a later stage or accelerated the proliferation of immune cells wrongfully trained to recognize self as the enemy. That, plus the chance that the problem EBV alerted the body too in the acute mono faze not being cleared may near permanently shift the immune state to a “pro ME” state.

    Its just a thought experiment but it shows how looking at the potential other side of EBV, the beneficial one it has in order to compensate for its nasty one and so to keep its host sufficiently healthy for its own survival, may learn more about EBV, ME and how to help bend conditions so that ME has less “feeding ground”.

  • Crystal

    July 6, 2019 at 12:12 pm - Reply

    Dejurgen, you are somewhat highlighting part of the point I was trying to make. That these viruses are such a part of our own immune system at this point that we may need to look at them in a different way, that they need to simply be eradicated or even brought down in numbers necessarily. I think in a nutshell that is what this whole article/research topic is showing

  • Crystal

    July 6, 2019 at 12:15 pm - Reply

    I meant to say that they DON’T necessarily n Ed to be eradicated. This is why I never leave comments ( because my typos are so bad! ) But this feels very close to home these days

  • Betty Mekdeci

    July 6, 2019 at 1:36 pm - Reply

    I think it is useful to move away from thinking about ME/CFS for a minute and consider the other conditions where opportunistic infections like EBV become a problem: organ transplants, chemotherapy for cancer, HIV infection and genetic immune deficiency syndromes. The famous “bubble boy” who was born without an immune system died when he was given a stem cell transplant from his sister. She had a mild EBV infection in early childhood, but when her stem cells were transplanted into her brother who had no immune system, the EBV caused cancer and killed him. I think my first doctor (now deceased) was right on target when he said that the immune system had to be boosted to control all of the pathogens reported in ME/CFS. The big question is what is causing the primary immune dysfunction?

    • Cort Johnson

      July 6, 2019 at 3:29 pm - Reply

      Agreed and some studies do suggest some people with ME/CFS have more difficulty fighting off EBV infection. Kerr’s study suggests EBV may be triggering the overactivation of immune genes in some as well.

  • dejurgen

    July 6, 2019 at 9:24 pm - Reply

    @Crystal, I already thought the brain fog ran away with the “don’t”.

    In pre industrial societies I would not be surprised if the preferential EBV “status” would be, in order from best to worst top to bottom:
    1) having EBV infection at young age
    2) never have EBV infection during lifetime
    3) having EBV infection at adult or worse late adult age
    Now, number 3) should still be the worst. About the position of 1) and 2) there I do doubt more. Evolution may have created a somewhat symbiotic relationship between humans and EBV in the past, but evolution only tends to adapt to known threats well. Adapting for a vastly changing lifestyle and diet plus encountering exotic foods and insects plus countless new chemicals that never existed before may require quite a lot more time, for both humans and this potential “relationship” with EBV.

    “Interesting thing is that everytime I “kill” viruses, whether with pharmaceutical antivirals or “natural” ones such as lysine I have a SEVERE mental/depressive and I mean severe, that is very unusual for me , reaction. Like I can literally feel the neuroinflammation.”

    Are you specifically aiming at viruses that can live lifelong in the human body or do you use therapies that also target these viruses? Lysine for example has a disputed role in fighting Herpes Simplex Virus according to wikipedia.

    If you would be targeting non-permanent viruses, have you considered an approach that does not effect the Herpes family and that does not change the immune setting?

    Having less of those “other” viruses might reduce the load on the immune system and reduce reactivation of Herpes / EBV.

    I use Isoprinosine (imunovir) in low dose and it helps me quit a bit. It doesn’t directly fight EBV which I have but it changes immune strength. But changing immune strength is a tricky thing to do that can go both ways.

  • Cort Johnson

    July 11, 2019 at 12:41 am - Reply

    It’s clear that EBV when encountered at an early age is easily fought off. That’s because the immune system is better adapted to fight it off. It’s almost as if it expects it to be there and when it’s not there – defenses weaken over time.

    I would be surprised, though, if the much harder fight against EBV during adolescence has anything to do with EBV “alerting” the immune system to other issues. By that time the immune system has simply lost some of its defenses – which not only results in a much longer fight but a higher risk of autoimmune disease. A shortened lifespan because of an autoimmune disease or cancer is counterproductive to EBV but evolution is not perfect and sometimes EBV will go too far – and kill or limit the ability of the host to pass it on. If EBV is a major player in ME/CFS – it’s surely done this by inhibiting its host so much that they don’t get out enough to pass it on.

    EBV dUTPase could very well be a mistake which does not help EBV at all but EBV doesn’t have to be perfect to survive – all it needs to do is inhabit enough bodies and move around enough.People with ME/CFS may be entirely immaterial to EV’s survival.

  • Michelle

    July 13, 2019 at 11:03 am - Reply

    Donna, you are misinformed and suggest you read his book. I have been following his plan to eradicate the ebv for the last 6.months and I can say with confidence my ME is 60% better. The reactions my body has given put also proves his theory and there is much more involved than just drinking celery juice.

  • patty

    August 24, 2019 at 1:50 pm - Reply

    fighting what I believe to be ep. barr but can’t get accurate and correct protocol. Yes, read Anthony’s celery juice advice. (His books are not designed for an idividuals specific case) I believe my thyroidectomy was due partly to this also.
    My story is long so need a good ear and sound advice…thanks !!!