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Are Infections Just a Trigger of ME/CFS, or an Ongoing Cause of ME/CFS?

Discussion in 'General ME/CFS Discussion' started by Eeyore, May 11, 2015.

  1. Eeyore

    Eeyore Senior Member

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    Note: This thread was split from this point in the thread: I need help--just left hospital with a deadly drug--hence no proper opening post.

    I do not believe that ME is an infectious illness. I believe it often begins with an infectious (or other) trigger but I do not believe ME is a persistent infectious state.

    I think patients tend to believe that because they felt good, got a virus, and didn't recover - but that doesn't mean that there is ongoing infection.
     
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  2. Hip

    Hip Senior Member

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    How would you interpret Dr John Chia's research which found significantly enteroviral infection in the gut tissues of ME/CFS patients, and when he treated these patients with IV interferon, many got full remission from ME/CFS, a remission lasting as long as 14 months in some cases, along with a simultaneous large reduction in enteroviral levels in their gut tissues.
     
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  3. JPV

    JPV ɹǝqɯǝɯ ɹoıuǝs

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    I believe that viral infections are a secondary opportunistic condition, or perhaps a trigger event, but not the root cause.

    I have no clue what the root cause might be, but If I had to venture a guess, I would say that it's about exposure to a conglomeration of environmental toxins coupled with a genetic predisposition to have a weak detox/immune system. Hence why this condition is so relatively new. It seems to coincide with the explosion of all the negative byproducts of industrial society. Modern drugs, such as antibiotics, may very well play into all of this by further harming our immune systems.
     
    Last edited: May 12, 2015
  4. Eeyore

    Eeyore Senior Member

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    @Hip @JPV

    Dr. Chia's research suggests that the immune systems of ME patients don't control infections as well as in normal people. Usually it seems that these are viral, although a UTI would likely be bacterial (if it responds to antibiotics, then definitely).

    Hepatitis C is a virus that many people acquire and spontaneously clear, while others do not clear it without treatment, and some don't clear it even with treatment. The traditional treatment for it is interferon (+ ribavirin). There are some newer treatments now that work better. Enteroviruses do not generally cause persistent infection. Even Dr. Hyde, who believes that enteroviruses are the most likely/common trigger for ME, said that they have never succeeded in isolating one after 3 yrs of infection. He did, however, isolate a virus similar to echovirus 25 in a substantial cohort of patients, and much further out in time that would be normal - and in family members who recovered, the virus was not found after the initial infection. It's possible some viruses are more persistent though - but it doesn't explain why a whole family gets sick, 3 get well, and one gets ME. Something is different with the immune system, and it goes against what we know about the infectious cycle for enteroviruses.

    Also, antibiotics are very effective at eliminating UTI's. If in fact you had to keep taking antibiotics for it, then it sounds like your immune system wasn't controlling it well (although that's peculiar because most evidence in ME points towards a Th2 shift and impaired cellular immunity - so you'd expect normal bacterial immunity).

    If the root cause of the problem is the enterovirus, then why can't Dr. Chia achieve permanent cure? Enteroviruses are not like herpesviruses - they are not lifetime infections. You get it, it runs its course, and it's gone. Polio is an example - it can leave major long term damage in some cases, but the virus itself is gone, there is no ongoing infection. Even in post polio syndrome, which they used to think might be an infection, they've never succeeded in isolating virus, even from tissue after death. All evidence points to it being long term damage from the virus, not reactivation or ongoing infection.

    I had a very classic onset with what I believe was probably an enterovirus (due to symptoms and season - June). Also I tested negative for mono at the time and all my other tests have not identified a pathogen, even in terms of past exposure - and much of the workup was around the time I first got sick. I do believe that enteroviruses are common triggers, but that's all.

    If there were an infectious virus in all ME patients, we'd have found it by now. Also, Dr. Chia would find the same virus or group of viruses in all patients, and he hasn't. Just as some people get sick after what is clearly an EBV infection, and others get sick after lyme, and still others after toxic exposures (e.g. organophosphate pesticides), enterviruses can trigger ME.

    Do you mind my asking which interferon you took (or which Dr. Chia uses)? I suspect ifn-gamma would make you worse, but class 1 interferons (alpha / beta) are less clear in their effects, and might even be helpful as immune modulators (maybe...) beyond their role in clearing viral infection.

    JPV - I doubt that antibiotics are the cause of this. Some environmental toxins may be relevant - e.g. pesticides. I got ME and was not taking any antibiotics around that time, or really for quite some time before then. I didn't get sick much before that. I had been up for a week studying for finals and pretty stressed, but had come home to my parents' house for summer when I got sick, and it was a few weeks after I got back.
     
  5. JPV

    JPV ɹǝqɯǝɯ ɹoıuǝs

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    It's believed that antibiotics can severally disrupt the bicrobiome. To my way of thinking, this makes it one of the potential trigger events, or at least complicating factors, but certainly not the only one. I don't think that there is a single identifiable cause for everyone. I think this is why we have so many subsets, that respond to different treatments, and why pinning down a single biomarker has proven to be so elusive.

    Like I said, I suspect genetic predisposition to be one of the main factors in all of this. Our systems have never had so many negative environmental health factors to contend with as they do now. Seems that some of us just don't have robust enough detox/immune systems to deal with all of it. I imagine that our bodies will never be able to evolve at the same rapid rate that our environment is changing.
     
    Last edited: May 12, 2015
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  6. Eeyore

    Eeyore Senior Member

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    I do think you're right that antibiotics alter the microbiome and that that may be an issue modern humans deal with regularly now. It's a reason antibiotic overuse is a bad idea. I don't think it's an ME trigger in particular, but who knows ... and there is such variability between people.

    I agree that the root is genetic. It would be interesting to know if in fact the incidence really is increasing or it's just recognized more. It goes back to at least the 30's (the LA hospital outbreak), but probably earlier (neurasthenia). I don't know about how common it was though.
     
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  7. Hip

    Hip Senior Member

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    What's you view on the types of ME/CFS in which viral or bacterial infection can be considered a proven cause, such parvovirus B19-caused ME/CFS, Chlamydia pneumoniae-caused ME/CFS, or Coxiella burnetii-caused ME/CFS?

    Because effective antivirals and antibiotics are available to treat these infections, you don't often get chronic cases of these types of ME/CFS. Nevertheless, these are cases of ME/CFS known to be caused by these pathogens.



    Certain enteroviruses definitely do cause chronic infections. Certain enterovirus species such as coxsackievirus B and echovirus form long term persistent infections in body tissues which are associated with various diseases.

    For example, chronic inflammatory heart disease (chronic myocarditis), which can later turn into a more advanced condition called dilated cardiomyopathy, is associated with chronic coxsackievirus B infections in the heart muscle (although CVB is not the only infection that appears to cause chronic myocarditis). These chronic coxsackievirus B infections are of the non-cytolytic form. Unlike regular enteroviruses, non-cytolytic enteroviruses live inside human cells, where they are not so easy to detect or treat.

    Some researchers (Prof Nora Chapman, Prof Steven Tracy) think that the persistent non-cytolytic coxsackievirus B infections found in chronic myocarditis may be a good model to study, in order to better understand the persistent coxsackievirus B infections found in ME/CFS.

    More info on how chronic coxsackievirus B myocarditis may be a good a model for studying enterovirus-associated ME/CFS can be found here: Human Enteroviruses and Chronic Infectious Disease.


    Chronic coxsackievirus B or echovirus infections have also been found in the pancreas in type 1 diabetes, in the muscle disease called polymyositis, in the motor neuron disease amyotrophic lateral sclerosis, and several other diseases.

    Definitively proving that these chronic coxsackievirus B or echovirus infections actually cause the diseases that they are associated with is something that takes much more research; but what is beyond doubt is the fact that these enteroviruses do cause chronic infections in the body.


    Numerous studies dating back to the 1980s have found enteroviruses in ME/CFS patients. See this long list of studies which found enteroviruses in various tissues of ME/CFS patients.

    In chronic coxsackievirus B and echovirus infections, it can be difficult to isolate and then culture the virus, simply because in chronic infections, enteroviruses tend to live in the non-cytolytic form inside human cells (ie, an intracellular infection), and this non-cytolytic infection does not produce any viral particles which are required for culturing a virus. However, you can detect the presence of non-cytolytic enterovirus infections by enterovirus RNA found in the infected tissue.

    Perhaps you are not aware of the relatively recent discovery of these non-cytolytic enteroviruses? These are the long sought after explanation of why you can find enteroviral RNA in certain chronic enterovirus infections, but often no infectious viral particles can be isolated. It's because often almost no viral particles are made in these non-cytolytic infections.

    Some info about non-cytolytic enteroviruses can be found on this thread. There are many other threads on this forum which discuss non-cytolytic enteroviruses, and how they might be targeted and killed.


    It is quite normal for viruses to produce severe disease in one person, but no symptoms whatsoever in the next. For example, when poliovirus was about, before vaccination eradicated it in the West, 90% of children who caught this virus were completely asymptomatic: the virus had no effect of them at all. But around 0.5% of children who caught poliovirus developed the paralytic symptoms of poliomyelitis, and out of those, a few percent would die (ref: here). So the same virus can be entirely asymptomatic or cause death, depending on the person.

    Similarly, Epstein-Barr virus is strongly linked to multiple sclerosis, but in spite of the fact that around 95% of the adult population have EBV in their body, only small percentage get MS.

    So there is nothing unusual about the same virus causing disease in some people, and no disease at all in others.

    Though certainly it is of great interest to understand why enteroviruses precipitate ME/CFS in some people but not others. I am very interested in what factors, alongside the enterovirus infection, are required for ME/CFS to appear.

    One of the discoveries Dr Chia made is that if the immune system is suppressed by corticosteroids during the acute stage of an enterovirus infection, this appears to be a good recipe for creating ME/CFS. See this thread. So conceivably, a weak immune system at the time of first infection may play a critical role in the subsequent development of ME/CFS. But this is likely not the only factor that may play a role in who gets ME/CFS and who doesn't from an enterovirus.

    Enteroviruses are also linked to precipitating autoimmunity, so if you have an ongoing enterovirus infection in your body, this may be driving an autoimmune response, which may well be part of the overall picture of ME/CFS.


    Where, can I ask, did you read that enteroviruses do not form chronic, permanent infections? Enteroviruses such as coxsackievirus B and echovirus are well known to form lifetime infections. Though other enteroviruses such as coxsackievirus A, enterovirus 71, and of course rhinoviruses, are only known to cause acute infections.


    I don't think anybody is saying that enteroviruses are the only cause/association of ME/CFS, not even Chia. As mentioned earlier, there are other known causes of ME/CFS, such as parvovirus B19 or Chlamydia pneumoniae. Chia treats a lot of patients whose ME/CFS appears to be caused by Chlamydia pneumoniae (this is a quite treatable form of ME/CFS, as is parvovirus B19-caused ME/CFS).

    And there are many ME/CFS cases that appear immediately after EBV infection, which may well be caused by EBV, although definitive evidence for a causal role of EBV in these cases has not yet been demonstrated.

    After mononucleosis, which is mostly caused by EBV, ME/CFS is found as a sequelae in around 9% of cases (ref: here).


    I have not taken interferon myself, and it's generally not really worth taking it for ME/CFS, due to the immense cost, significant side effects, and the fact that the enterovirus infection does not get eradicated, and so later returns. Chia experimented with interferon some years back, but I understand he rarely uses interferon now (except in certain circumstances). Rather Dr Chia uses immunomodulatory approaches such as oxymatrine. I am not a patient of Dr Chia, but have read a lot about his research.

    Some info on the various types of interferon Chia experimentally used is given here (see about half way down on page).

    Type I interferons are the only ones that can target the intracellular non-cytolytic enterovirus infections that Chia and others think likely plays a major role in enterovirus-associated ME/CFS.
     
    Last edited: May 13, 2015
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  8. JPV

    JPV ɹǝqɯǝɯ ɹoıuǝs

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    Unfortunately, I think ME/CSF has become a grab bag of conditions that don't neatly fit into any other single category. Hence why we are always discussing subgroups and why one treatment is helpful for one group but may be disastrous for another.

    As you've acknowledged, the Parvovirus B19 pertains to just one subset. Either way, I don't think this contradicts my belief that environmental factors may contribute to impairing individual detox and immune systems which then allow for easier and more debilitating infection by opportunistic pathogens.

    Here's some info regarding Parvovirus B19 which supports my view that viruses like this are likely opportunistic infections in at least some subsets of ME/CFS patients...
    And this, from Ian Lipkin, regarding toxins in our modern enviroment...
     
    Last edited: May 12, 2015
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  9. Eeyore

    Eeyore Senior Member

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    @Hip -

    I don't believe any cases of ME are known to be caused by any pathogen. Triggered, yes, caused, no. I would suspect that EBV induced ME would be more persistent and have a worse outcome since the virus is never eliminated, therefore it might continue to trigger the disease process on an ongoing basis - however, a very recent study showed the opposite - that EBV-triggered ME has an excellent prognosis. I don't understand why this is the case.

    I think we may be defining chronic/persistent infections differently. I think of chronic infections as being more like HIV or herpesviruses - i.e. for life. This is not the general understanding of how enteroviruses work. It may be that in a few cases, in people with severe immune dysfunction, what would normally be cleared could become chronic, but I've never seen anything very convincing. If you have a link to published research I'd be happy to look at it, but it's definitely against conventional medical understanding of enteroviral infections - they are viewed as infections that either you clear or that kill you. Coxsackievirus B3 is, as you mention, a cause of cardiac infection and ultimately, in some cases, DCM. B4 is associated with diabetes. Usually, however, most of the damage occurs early on, and there may then be a low level persistence of a virus in a non-lytic cycle, but eventually the infection is cleared. Even then, it can stimulate an autoimmune response which probably plays some role in long term disease progression. Sometimes it can take years to clear enteroviral infection (probably up to 3 or so).

    I'm not sure I believe in the existence of persistent, non-lytic enteroviral infection. I can't rule out the possibility, but it doesn't really seem to fit with our understanding of how the viruses work. For one, they cannot incorporate into cellular DNA, as they have no DNA at all. Herpesviruses can (they are DNA viruses) and so can HIV or other retroviruses - they can convert their genomes to DNA with reverse transcriptase. At no point in the enteroviral life cycle is it DNA.

    Therefore, where is it stored? How does it exist over the long term without triggering normal cellular responses? RNA should be triggering various PRR's / TLR's. Protein Kinase R would be triggered, MHC expression would be upregulated, etc. It doesn't seem to make basic virological sense. That doesn't mean it can't happen, but rather that I'd have to see a lot of evidence before I was convinced, and a lot of questions would have to be answered. In humans, viruses that have lytic and lysogenic cycles generally can insert into DNA - and there is no way to do that with enteroviruses.

    Also, in interpreting Coxsackievirus antibodies, the body actually stops making them pretty early after infection, suggesting there is no persistence of antigen. This is also inconsistent with persistent infection. People who do develop Coxsackie B3 related myocarditis usually get really sick really fast, and then recover over a period of several years (although some die or require heart transplant). It doesn't seem to follow any kind of long term stable pattern. I've never heard of a case of recurrence after heart transplant, even with post-transplant immunosuppression, also arguing against persistence of replication-competent virus.

    We are in full agreement that there are many pathogens that can trigger ME - however, we don't agree, it seems, as to whether or not infection is generally persistent. For one thing, ME is a syndrome with a particular, well defined set of symptoms that is easily recognizable to those who have worked with it. The pathogens you list would cause dramatically different syndromes. The fact that people with ME share symptoms implies shared pathology - some sort of immune dysregulation makes the most sense to me, and the research supports it reasonably well (or at least is consistent with it) - although the precise nature remains unclear. EBV doesn't look clinically like c. pneumoniae infection, yet ME triggered by each looks pretty much the same.

    All interferons target intracellular infection, although there are some differences and they are used for different diseases. Alpha is the most often used for viral infections in general in clinical practice.

    We don't know everything about viruses, but this is what we studied in my virology classes - so if you want to link me a particular paper I am open to new information. Everything I've seen though is that despite many attempts to show long term persistence of enterovirus infection, we have failed to do so. Yes, they can cause permanent disease states, but that is not the same as permanent infection.
     
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  10. Eeyore

    Eeyore Senior Member

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    @JPV - Interestingly, my view is somewhat opposite yours. I think that if there are environmental chemical effects, the problem is more immunostimulatory than immunosuppressive - but it's not clear exactly what.

    I tend to view ME as an immune overactivation rather than a weakened immune system (although that could mean overactivation of one part compensating for dysfunction of another).
     
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  11. JPV

    JPV ɹǝqɯǝɯ ɹoıuǝs

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    I actually agree with your point of view. It was probably a poor choice of words that implied that I believe the detox/immune system is weakened in ME/CFS. I think that it's much more complex than that. It could very well be some form of dysfunction that manifests as an over-active reaction to pathogens.
     
    Last edited: May 12, 2015
  12. Hip

    Hip Senior Member

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    @Eeyore
    You make some very interesting points, which I have had to think about, and do some Google research on.

    Were your virology classes part of a medical degree or similar, by the way?


    Just to make sure we are using the same terminology:

    I presume by the term trigger you mean something like viral "hit and run" damage to the body, or viral instigation of autoimmunity; and you also mean that once such triggering events occur, they cannot be easily undone; that is, there is a certain irreversibility about a condition or disease that a pathogen triggers.

    Whereas by contrast, if a pathogen is causing and maintaining a disease such as ME/CFS, I presume what you mean is that the disease only exists because the pathogen is still in the body, and still causing the disease on a day by day basis.

    In other words, if you could remove a viral cause from the body, the disease would disappear; but if you could remove a viral trigger from the body, the disease would continue.

    Would you say that is an accurate definition of what you mean by trigger and cause? That's generally how I use the terms trigger and ongoing cause.


    OK, well given this terminology, how would you then interpret the appearance of ME/CFS in some people on contracting parvovirus B19 or Coxiella burnetii, and the sudden disappearance of all ME/CFS symptoms on eradicating these infections with antivirals/antibiotics?

    If these infections triggered the condition of ME/CFS, then clearing the infection would not cause ME/CFS to disappear, because a trigger has this irreversibility.

    Whereas if these infections are causing and maintaining ME/CFS, then clearing them would result in ME/CFS being cured.

    So the fact that the ME/CFS disappears on clearing infections like parvovirus B19 or Coxiella burnetii suggests these pathogens are ongoing causes, rather than triggers of ME/CFS.

    Or can you suggest an alternative interpretation of this?

    I know few researchers seem to want to call parvovirus B19, Coxiella burnetii or Chlamydia pneumoniae known causes of ME/CFS (except Dr Chia, who entitled one of his papers as: Chronic Chlamydia Pneumoniae Infection: A Treatable Cause of Chronic Fatigue Syndrome); however, the evidence for a causal role seems reasonable to me.


    Similarly with enterovirus. Although you unfortunately cannot at present eradicate chronic enterovirus infections in ME/CFS, you can greatly reduce viral loads using interferon. Once the enteroviral loads are so reduced, you often find ME/CFS disappears, at least for a few months to a year, after which the virus returns, and so do the ME/CFS symptoms. One of Chia's papers on interferon treatment of ME/CFS is here, and he also talks about interferon in his major studies on enterovirus and ME/CFS here and here.

    John Chia got similar results with the immunomodulator oxymatrine: in some patients, this herbal extract dramatically reduced viral loads, and led to huge improvements in ME/CFS (you can see Chia's before and after pictures of stomach tissue enteroviral load reduction due to oxymatrine treatment in my post here). In patients who got much better but then discontinued oxymatrine, their ME/CFS returned.

    So to me these observations suggest that enteroviral and other infections are not a trigger of ME/CFS, but an ongoing cause, which once eradicated, leads to cure / remission of ME/CFS.

    Again, if you have an alternative explanation or hypothesis for this data, please do elaborate. To me it seems like reasonable evidence of a causal rather than triggering role of enterovirus (and the other above infections) in ME/CFS.



    I too am defining chronic/persistent infections as ones that stay in the body for life.

    I don't actual know how long CVB myocarditis and dilated cardiomyopathy can last, and whether they can last a lifetime, so I am not sure if these can be examples of a lifetime CVB infection.

    In adult type 1 diabetes, though, there are many studies that have found enterovirus / CVB / echovirus antibodies or RNA. I have just been looking through these, ignoring studies that examined recent-onset or juvenile diabetes (because the presence of enterovirus in these cases might just be a short-term presence), and instead I just fished out a few studies which found enteroviral RNA in longer-term diabetes patients. Some of these studies, listed as follows, are at least suggestive of a lifetime presence of this virus in the body:

    Type 1 diabetes is associated with enterovirus infection in gut mucosa
    Enterovirus infection and type 1 diabetes mellitus: systematic review and meta-analysis of observational molecular studies
    Detection of enteroviruses in the intestine of type 1 diabetic patients



    As you undoubtedly know, very few viruses can incorporate themselves into human DNA, and as far as I am aware, most lifelong viruses use genetic episomes as their latency mechanism.

    Though enteroviral non-cytolytic infections are not quite the same as a latency state; these non-cytolytic infections are active, albeit low-level "smoldering" infections.

    I have not come across any articles or studies indicating scientific doubt about the existence of non-cytolytic viral infections.

    I believe non-cytolytic infections are similar to (or possibly the same as — but I am unclear on this) defective interfering viruses. Dengue virus is an example of an infection that comprises both a defective interfering virus as well as a regular virus in tandem. See this article:

    'Defective' virus surprisingly plays major role in spread of disease, UCLA life scientists report | UCLA


    Non-cytolytic enteroviruses comprise both viral ssRNA and dsRNA, and live in the cell's cytoplasm. These RNA strands are able to resist eradication by the cell's immune system because:

    (1) dsRNA is very hardy, and the immune system has trouble destroying this.
    (2) ssRNA is easier to destroy; however, as is well known, the RNAse L enzyme responsible for destroying ssRNA is dysfunctional in ME/CFS patients (this enzyme is unfortunately cut up into smaller ineffective pieces in ME/CFS patients), so that make it harder to fight non-cytolytic infections. If you Google RNAse L chronic fatigue syndrome you'll find lots of info on this.

    Also, CVB3 down-regulates MHC expression in order to make infected cells invisible to CD8 T cell surveillance (ref: here).


    More info on non-cytolytic enteroviruses:

    This was a groundbreaking study of its time:
    Persistence of enteroviral RNA in chronic fatigue syndrome is associated with the abnormal production of equal amounts of positive and negative strands of enteroviral RNA

    The above study found that whereas in normal enterovirus infections in human cells, the positive strand RNA out numbers the negative strand RNA by around 100 to 1 (the -strand is the template, and the +strand the copies of the viral genome), in the muscles of ME/CFS patients, there was approximately equal the amounts of positive and negative strands. This is in fact characteristic of non-cytolytic infections, and what is thought to happen is that many of the positive and negative strands then join to form this very hardy dsRNA.

    If you want to search the Internet, using various synonyms for non-cytolytic enteroviruses, see here.



    As an aside: in EBV latency, partial reactivation can occur in some ME/CFS subsets, where some viral proteins are produced. So in ME/CFS, EBV may also be in active state, but without necessarily producing viral particles.


    I think the antibodies drop to a very low level soon after the acute infection, but I know that when Dr Chia uses ARUP Lab, he reliably finds antibody titers in ME/CFS patients. And several studies have found CVB / echovirus antibodies in a large percentage of the general population:

    This study found coxsackie B virus IgG antibodies in 55% of the population in Scotland. This study found coxsackievirus B pretty prevalent in the general population in Greece. And this study found various coxsackievirus B and echovirus species pretty prevalent in infants in Norway.



    Are you saying that in chronic disease states, you can find chronic CVB, whereas you don't think there is evidence for chronic CVB in healthy people?

    Certainly there is no question that you can detect enterovirus RNA in chronic CVB myocarditis, ME/CFS, and in type 1 diabetes.

    But if I understand you correctly, you are saying that there is no evidence for lifetime enterovirus infections in healthy people without diseases. By evidence, I presume you mean finding enteroviral RNA in the body (as opposed to enteroviral antibodies, which perhaps might persist even if the enterovirus infection was eradicated).

    OK, well I have been Googling on this, and all I have found so far in terms of evidence of chronic lifetime enterovirus in healthy populations is the following:

    • Many decades after being infected with poliovirus, around 30% of polio victims experience post polio syndrome later in life, and some studies have found poliovirus RNA in the CNS in these people (ref: here).

    • Long term persistence of coxsackievirus B infection in the brains of mice: mice infected with CVB as neonates still have the virus present as adults:
    Viral persistence and chronic immunopathology in the adult central nervous system following Coxsackievirus infection during the neonatal period



    Absolutely. If these diverse pathogens can cause/trigger ME/CFS, there must be a good explanation as to why they all produce very similar or identical ME/CFS symptoms and pathophysiology.

    The best theory I have come across with the power to explain this is Michael VanElzakker's vagus nerve infection hypothesis of ME/CFS.

    In case you are not familiar with this theory: VanElzakker points out that sickness behavior has very similar symptoms to those of ME/CFS, and that sickness behavior can be switched on by nerve signals sent to the brain via the vagus or trigeminal nerves, when either of these nerves sense infection and inflammatory cytokines in the body.

    VanElzakker hypothesizes that a chronic infection of the vagus nerve itself, from one of these ME/CFS-associated pathogens, would result in the vagus nerve constantly sending inflammatory signals to the brain, thereby permanently switching on sickness behavior, and thus constantly causing the symptoms of ME/CFS.

    In VanElzakker's theory, it's not so much the type of pathogen that is important; it's simply whether that pathogen infects the vagus nerve or not.

    Whether this intriguing theory is true or not remains to be seen. However, the remarkable thing about this theory is that it does offer an explanation of how ME/CFS may be caused/triggered by disparate pathogens, yet looks pretty much like the same disease in every case.
     
    Last edited: May 13, 2015
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  13. Sushi

    Sushi Senior Member Albuquerque

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    Thread has been split so bumping up.
     
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  14. Hip

    Hip Senior Member

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    Here is some more evidence that chronic enterovirus exist: see this study:
     
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  15. heapsreal

    heapsreal iherb 10% discount code OPA989,

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    Varicella zoster is rarely mentioned as a chronic infection. I never really thought of it as that either but my thinking is changing on this. My cfs onset where the straw that broke the camels was chickenpox as an adult and previously had it as a child.I also had cmv and ebv(around the cfs onset) but for some reason test neg to ebv. Testing i had was the usual herpes viruses without vzv. My dr and i assumed cmv, and i was only able to get 1 test of cmv with a titre value that would fit me into the reactivation group which dr lerner mentions. I think its possible i have both cmv and vzv running together. Theres been a couple of autopsies showing cfs/me people having zoster type lesions in their nervous system such as dorsal ganglion root.

    I have had the recent shingles outbreaks which messed me up, so researching into this further i did not realise there is a chronic form on vzv and it can show no rash called zoster sine herpete. So was it zosters sine i have had for many years and only recently shown a rash? Also mollarets meningitis which is a chronic form of meningitis from vzv and also commonly from herpes 1 and 2, other herpes viruses such as ebv/cmv/hhv6 can also cause this. I am following all this up with an immuno soon hopefully.

    I think the state of viral testing of active viruses is not very accurate, so i think many get undiagnosed because of this. Its probably also true that for some its a hit and run thing with infections. I dont thing we can really speak for all of us as a group but need to be individually worked up to find our own unique abnormalities.
     
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  16. halcyon

    halcyon Senior Member

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    Evidence for persistent enterovirus infections in ME:

    Galbraith DN, Nairn C, Clements GB. Evidence for enteroviral persistence in humans.
    Chia J, Chia A, Voeller M, Lee T, Chang R. Acute enterovirus infection followed by myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) and viral persistence.
    Chia JK, Chia AY. Chronic fatigue syndrome is associated with chronic enterovirus infection of the stomach.
    Chia JK, Chia AY. Ribavirin and Interferon-a for the Treatment of Patients with Chronic Fatigue Syndrome Associated with Persistent Coxsackievirus B Infection: A Preliminary Observation.
    Douche-Aourik F, Berlier W, Féasson L, Bourlet T, Harrath R, Omar S, Grattard F, Denis C, Pozzetto B. Detection of enterovirus in human skeletal muscle from patients with chronic inflammatory muscle disease or fibromyalgia and healthy subjects.
    Galbraith DN, Nairn C, Clements GB. Phylogenetic analysis of short enteroviral sequences from patients with chronic fatigue syndrome.
    Cunningham L, Bowles NE, Lane RJ, Dubowitz V, Archard LC. Persistence of enteroviral RNA in chronic fatigue syndrome is associated with the abnormal production of equal amounts of positive and negative strands of enteroviral RNA.
    Gow JW, Behan WM, Clements GB, Woodall C, Riding M, Behan PO. Enteroviral RNA sequences detected by polymerase chain reaction in muscle of patients with postviral fatigue syndrome.
    Archard LC, Bowles NE, Behan PO, Bell EJ, Doyle D. Postviral fatigue syndrome: persistence of enterovirus RNA in muscle and elevated creatine kinase.
    E. G. Dowsett, A. M. Ramsay, R. A. McCartney, E. J. Bell Myalgic encephalomyelitis--a persistent enteroviral infection?
     
  17. halcyon

    halcyon Senior Member

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    Besides what I posted above, there is research showing persistent enterovirus infections in humans causing chronic myocarditis. I won't bother posting all that, it's easily found on PubMed. There is also some thought (and perhaps some research though I haven't looked) that persistent poliovirus infection is behind post-polio syndrome. Also, people with agammaglobulinemia can develop persistent years long enterovirus infections. So yes, they don't generally cause persistent infection in healthy people as far as we know, but there is a mountain of evidence showing it can persist for long periods of time in a subset of the population and does cause disease.
     
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  18. halcyon

    halcyon Senior Member

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    If I recall correctly, @charles shepherd was diagnosed with ME (by Ramsay) after VZV infection. I think any pathogen capable of persisting that can infect nerve, muscle, and brain can cause ME.
     
  19. heapsreal

    heapsreal iherb 10% discount code OPA989,

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    Something i read recently stated that EV was the most likely cause of viral meningitis. The figures were something like 90% were probably caused by EV, the remaining were mostly hsv1/2 and the small remaining were the rest of the herpes family.
     
  20. heapsreal

    heapsreal iherb 10% discount code OPA989,

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    VZV doesnt seem to be seen in the same light as other herpes viruses like ebv/cmv/hhv6, almost like the forgotten herpes virus, especially for a chronic ongoing virus. I think its something to be aware of as a possible ongoing problem for some and good to rule out or in?
     
    merylg likes this.

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