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

[leokitten]

I think the idea is not that there is a unique virus that is capable of causing symptoms in everyone exposed, but that there is a double- (or triple-) hit situation going on or that some other factor impacts the severity of illness as the result of infection. Perhaps PWME have genetic immune problems that make them less capable of handling the virus than most people, or that it takes multiple stressors at the same time or in close succession to make a PWME susceptible to a more serious infection from the virus. It's possible we are not able to clear the virus the way other people do.

There are known examples of pathogens affecting people very differently -- even people in close contact. Think about EBV and Burkitt's or Hodgkin's Lymphoma. Very few people get either of those diseases as a result of EBV infection, but some do as a result of genetic factors or combined infections. Another example is polio. Many people get it and clear it without consequence, but others have mild-severe consequences. IIRC, the factor is what tissues get infected. For example, my cousin is quadriplegic as the result of polio while her brothers who got ill at the same time have no known consequences from the infection.

While those cases are hit-and-run situations, it's not beyond the realm of possibility that any number of factors, immune dysfunction or location of infection for example, might make an infection enduring (or reactivating) in some people but not in others.

I completely understand this and agree with this as a possibility, but what @Hip and @unto have stated is something a quite different, that they are passing a virus that seems to affect a lot of people around them in a significant and long-term way.

 

[Hip]

The question I ask myself is, if there is indeed a virus causing ME/CFS and other major problems that is as easily transmittable and causes the very significant symptoms in most people that you've stated wouldn't there be a widespread epidemic of people with these symptoms? All the people you've supposedly infected are contagious and infecting others, and they further infect others, and so on exponentially, and the symptoms are quite serious.

Those were my exact thoughts when I first caught my virus, this idea that my virus might spread exponentially like a global influenza epidemic, and cause havoc worldwide. My virus was not very contagious: one person with my virus would take around a year to infect all the other members of his household; but I observed the contagion to all other householders was almost guaranteed once one household member had the virus. So I thought, well, it may take a decade or two, but my virus will slowly spread to the whole world.

However, after reading something about enterovirus epidemiology, I learnt that enterovirus outbreaks don't work like that. They do not undergo long-term exponential growth. Enterovirus outbreaks of coxsackievirus B or echovirus will grow bigger and bigger over the course of a few years, but then instead of continuing to grow, they will start to fade away. Nobody quite knows why this is. Of course there are quite a few serotypes of coxsackievirus B and echovirus, so when one outbreak fades away, another may start.

Why do so many people with ME/CFS have wives and husbands with no health problems? (including my own)

It is possible that not all enteroviruses spread like mine did. One characteristic of my virus is that it would cause a permanent sore throat in around ⅓ of people who caught it, and permanent nasal inflammation and overproduction of nasal mucous (meaning you have to keep blowing you nose) in around ⅔ of people who caught it. I think both these ongoing respiratory infections/inflammations, are likely constantly shedding viral particles in the saliva and mucous, making people with my virus possibly permanently contagious to others. I think these permanent respiratory infections enables my virus to spread to many.

However, if the enterovirus you catch does not cause these permanent respiratory infections, it may not so easy transmit from you to others.

In a sense, my chronically contagious virus provided the perfect opportunity to observe the effects of a ME/CFS-triggering virus on the general population. And as I mentioned, in the 30+ people I know who caught my virus, nobody developed full ME/CFS like me, but many people permanently developed certain symptoms that you find in ME/CFS, like such as increased fatigue, sound or light sensitivity, or "tip of the tongue" phenomena where you temporarily forget a common word or person's name.

So from the evidence I gathered as my virus spread to many people, it became clear to me that elements of ME/CFS can appear in lots of people that catch an enterovirus. I just think I may have had certain factors present in my body that made the virus hit me much harder than anyone else, explaining why I permanently developed full ME/CFS, but everyone else who caught my virus were just hit with one or two mild (though permanent) ME/CFS symptoms.

But make no mistake, it was abundantly clear that my virus is capable of producing these mild ME/CFS symptoms in a lot of people.

So that is something that I think needs to be taken on board in this discussion.

 

[Hip]

And let me say that these various symptoms I observed in the 30+ people infected with my enterovirus were very similar to the symptoms that the GP John Richardson observed when coxsackievirus B infections spread in the families he was treating:

To re-quote what I posted earlier on Dr Richardson's observations of coxsackievirus B spreading through families:

The clinical features of these infections varied from Bornholm disease—a common short illness with chest pain—to audible pericarditis, serious myocarditis, and valvulitis with dysfunction. Other features were muscle pain, jitter and weakness, sleep disturbance, hypersensitivity to sound and light, and mild confusion.

Many organs in the body could also be affected. In the long term the effects were sometimes serious. While some members of a family would escape with a brief febrile illness only, coxsackie infection could leave one person struggling for years with ME or dilated cardiomyopathy.

Worse still, John found that the infection would readily pass from the mother to her unborn child, which would be delivered with fibroelastosis or maldevelopment of the heart, or structural defects of the brain or other organ. He tried to prevent this in early pregnancy by giving the mother intramuscular injections of human immunoglobulin.

 

[SOC]

I completely understand this and agree with this as a possibility, but what @Hip and @unto have stated is something a quite different, that they are passing a virus that seems to affect a lot of people around them in a significant and long-term way.

I have to agree that it is unlikely that most PWME have a contagious virus that is routinely seriously infecting other people. Our ME/CFS specialists seem to agree with that thinking as well.

That isn't to say that any individual PWME might not have a contagious infection, just that it's not universal, or even common.

 

[Hip]

@SOC
I think human beings in general are constantly infecting each other with various pathogens, but most people are not observant enough to notice this.

To give you an example, I never thought much about it at the time, but once in my early twenties, when I started going out with a new girlfriend, very soon after commencing sexual relations I developed, completely out of the blue, the condition of overactive bladder (OB) syndrome. This disease appeared within weeks of starting sexual relations.

Overactive bladder is a condition where you badder muscles become "nervous", and this produces strong, sudden urges to urinate. OB is similar to interstitial cystitis (IC), but without the pain of IC. So suddenly all day I found myself rushing between one toilet and the next; whereas prior to that, I could go almost a whole day without once needing to visit the toilet, as my bladder was very strong.

At the time I never really thought much about why OB suddenly appeared, but in retrospect, with the medical knowledge I have acquired since developing ME/CFS, I think that the most likely explanation for my sudden development of OB was that I contracted some sort of infection from my girlfriend. Given the precise timing, nothing else seems to reasonably explain it.


In general, I suspect that many diseases we suddenly inexplicably get may be the result of acquiring a pathogen from another human being, or sometimes from the environment, but people never put two and two together, partly because the initial contraction of a pathogen can be asymptomatic.

If you have ever read any of the numerous stories online of various ill health conditions that men have picked up from visiting prostitutes (I am not talking about standard STDs, but rather systemic illnesses and systemic ill health), you will begin appreciate how disease causing pathogens are constantly passed between humans.


Hopefully one day we will have an advanced technology that will automatically detect whenever we have caught a new pathogen. Something like a high tech wristwatch that monitors the blood for the appearance of new antibodies. Then people will become aware of when and what they have caught, and will be better able to relate the acquiring of a new pathogen to the subsequent appearance of a disease.

If we had such a wristwatch, I think there would be no doubt as to the viral etiology of ME/CFS, as we would then have access to a digital database of millions of cases where ME/CFS followed specific pathogenic infections.

 

[msf]

I thought this paper might be relevant to the earlier discussion of sickness behaviour and ME: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3751187/

If someone already posted this, sorry but I wasn't going to go through 24 pages of comments again!

 

[unto]

hello to all and all,
I'm sure now that (my) ME I can pass it even now after 30 years from the start on my body ....., I would bring some clues, maybe for some of you "worthless" to be reckoned with.
I state, I am convinced that the ME is widespread around the world (approximately 5% of the population, perhaps), only that the seriously ill are a very small percentage.

Are many decades that the germ (virus?) Affects humans, so having regard to its cunning in evading our immune system (not causes severe inflammation ......) is very likely to be further adapted in order to infect more people but cause less severe cases of ME.

The severity of ME may be due to a mix of factors (as says SOC)
the health history of the patient, from which and how many other germs met his body, from his genome, the state of her immune system when she contracted ME
believe, however, that only the severity of the disease depends on this, because the 99% whoHe meets that germ
(or family of germs)
contracts the ME .....


I have always worked, even 10 hours a day, of course, with great effort, after lunch almost collapsed from sleep ......, now for some years no longer work, but I struggle even more ..... (sometimes ), this is to say that the new generations of sufferers could hardly feel the disease ......; as years ago it was thought that they were not affected children and over sixty ...., how could they make the children to convince and persuade parents and doctors who were evil, could only be "difficult children" to be treated with Prozac ... ., and to the beat of the sixties was enough primary care physician, "you're getting old," are warm and take a Tavor ......After 30 years of illness I saw dozens of people who have contracted the ME because of me, the first few years I lived in anguish and guilt, it is very difficult to accept that the people you best (family, relatives, friends, partners, colleagues) suffer because of you and you can not eventell him .......Well all these people only one is in a pitiful state, and it is so not because of ME directly, but because it was not supported adequately in the family and was not able to process thoughts and actions appropriate.

I do not know if you also you realize that in the world of advertising we are inundated with pharmaceutical or herbal cure for: Mel's head, sore throat, fatigue, memory, intellectual capacity, etc ...
I believe that this is also a sign that the ME has spread very .....
the multinational drug companies know more than many doctors ........ and also insurance
that if you say that you do not provide the ME .....
it is late good night

 

[Hip]

@Jonathan Edwards

Returning to the vagus nerve infection hypothesis discussed earlier in this thread:

The idea that it could be a chronic stomach infection (rather than an infection within the nerve itself) that the vagus is detecting looks very feasible, for the following reasons.

If you examine John Chia's study on the chronic enterovirus infections of the stomach found in ME/CFS patients, you see that it was specifically the parietal cells of the stomach which were infected with enterovirus.

Now it turns out that parietal cells are directly innervated by the vagus nerve: it says here that:

Acetylcholine is released by parasympathetic fibers in vagus nerve efferents which synapse directly onto parietal cells.

(Although note that here it says the vagus does not innervate the parietal cells directly, but synapses with ganglion cells of the ENS — so I am not entirely sure what is going on).

But if the vagus is indeed synapsing onto the parietal cells, presumably this might place the vagus sensory neuron IL-1β cytokine receptors in very close proximity to the parietal cells, such that these receptors would be constantly activated by any IL-1β cytokines released by enterovirus-infected parietal cells.

Though I am a bit unclear on the anatomy, because the parietal cells would be innervated by the efferent branch of the vagus nerve, and the sensory neurons will be on the afferent branch of the vagus nerve. So I am unclear just how close the vagus sensory neurons will be to the parietal cells.


Thus even if the vagus nerve is not itself infected in the way VanElzakker originally suggested, with this chronic parietal cell infection in the stomach, exactly the same principle that VanElzakker proposed in his paper could still apply: namely that cytokines from a chronic parietal cell infection — cells which are in very close proximity to the vagus — are constantly activating sickness behavior, leading to ME/CFS symptoms.

In this slight variation of VanElzakker's theory, we do not have to speculate which cells may or may not be infected, as we know from Chia's stomach biopsy work that the parietal cells are infected with enterovirus in 82% of ME/CFS patients.

So this variation of the theory fits well with the data.

 

[jepps]

@Jonathan Edwards

Returning to the vagus nerve infection hypothesis discussed earlier in this thread:

The idea that it could be a chronic stomach infection (rather than an infection within the nerve itself) that the vagus is detecting looks very feasible, for the following reasons.

.

http://medicalxpress.com/news/2015-06-parkinson-disease-gut.html

Our study shows that patients who have had the the entire vagus nerve severed were protected against Parkinson's disease. Their risk was halved after 20 years. However, patients who had only had a small part of the vagus nerve severed where not protected. This also fits the hypothesis that the disease process is strongly dependent on a fully or partially intact vagus nerve to be able to reach and affect the brain

Parkinson could also be related to an infection of the vagus nerv.

 

[Tammy]

And if I'm not mistaken more and more evidence is showing that EBV is more intricately involved in the demyelinating autoimmune process than previously thought.

When diagnosed I had extremely high EBV titers and I believe the EBV did some major damage. An immunologist did some really good lab tests (wish I still had them) and one of the lab results showed myelin antibodies. I have a numbness that covers my entire body...........not a complete numbness.......I can still feel hot and cold but my feeling is "muted" for lack of a better term. The numbness started off in patches on my body and then finally covered my entire body. This was extremely scary.............now I'm used to it...........feels like my body is wearing women's stockings..........thank god the damage did not progress.

 

[Violeta]

When diagnosed I had extremely high EBV titers and I believe the EBV did some major damage. An immunologist did some really good lab tests (wish I still had them) and one of the lab results showed myelin antibodies. I have a numbness that covers my entire body...........not a complete numbness.......I can still feel hot and cold but my feeling is "muted" for lack of a better term. The numbness started off in patches on my body and then finally covered my entire body. This was extremely scary.............now I'm used to it...........feels like my body is wearing women's stockings..........thank god the damage did not progress.

@Tammy What did you do to stop the progression?

And have you seen this site? http://selfhacked.com/2014/06/27/homing-fundamenal-cause-epstein-barr-reactivation/

 

[Violeta]

And if I'm not mistaken more and more evidence is showing that EBV is more intricately involved in the demyelinating autoimmune process than previously thought.

This article says it's involved in other autoimmune diseases, too.

http://www.hindawi.com/journals/jir/2013/535738/


Thank you for that information. I wonder if that's what happens to the vagus nerve?

 

[Violeta]

I think that maybe EBV might turn into MS when there's a metal involved. First and foremost I'm thinking mercury. Let me search to see if this is just an opinion or knowledge.


https://www.hugginsappliedhealing.com/

 

[barbc56]

Way to wooish, at least for me. Some very unscientific as well as dangerous treatments.

Natural oncology? Ridiculous, IMHO!

Barb

 

[Tammy]

@Tammy What did you do to stop the progression?

And have you seen this site? http://selfhacked.com/2014/06/27/homing-fundamenal-cause-epstein-barr-reactivation/

I've tried so many things I really don't know what I was taking back then.......it's all a blurr. I did take a look at the link. I've been back and forth about EBV and whether or not after 19 years it is still a factor..............do I pursue antivirals or not is what I've been tossing back and forth ............I'm sure I've tried them in the past..........but my memory has failed me.

 

[Violeta]

I've tried so many things I really don't know what I was taking back then.......it's all a blurr. I did take a look at the link. I've been back and forth about EBV and whether or not after 19 years it is still a factor..............do I pursue antivirals or not is what I've been tossing back and forth ............I'm sure I've tried them in the past..........but my memory has failed me.

Did you try herbal antivirals or drugs? I've been doing so much better since I started taking lomatium, echinacea, some olive leaf extract, and drinking cistus incanus tea. I also have been taking some colostrum. I don't see any possible downside from doing these things, either.

 

[Violeta]

(although that could mean overactivation of one part compensating for dysfunction of another)

Wow, I do think that really nails it!

Although I might change one or two of the words, I just don't know what I would change them to.
Maybe it's not a compensation by a ___________? Don't know what word to put there.

This might be an underactive or dysfunctional arm of the immune system:
*ME scientists believe that this CD8+ T-cell deficiency underlies the development of chronic autoimmune diseases by not controlling Epstein-Barr virus (EBV) infection. "

This would be the overreactive part:
*"If EBV isn’t controlled, it can wreak havoc on the body. When EBV infects B cells it can make them “autoreactive”, which means its products (antibodies) target our own tissues."

*Quoted from selfhacked.com

 

[Hip]

Our study shows that patients who have had the the entire vagus nerve severed were protected against Parkinson's disease. Their risk was halved after 20 years. However, patients who had only had a small part of the vagus nerve severed where not protected. This also fits the hypothesis that the disease process is strongly dependent on a fully or partially intact vagus nerve to be able to reach and affect the brain

Parkinson could also be related to an infection of the vagus nerve.

That is an interesting study, and I posted some thoughts about it (in the context of ME/CFS) here.

 

[halcyon]

Let's go over some of the past autopsy findings on ME patients.

Behan, Gow, and Mcgarry published findings from a patient that committed suicide. Sadly the full text isn't available, there is only this excerpt:

Sadly no mention of any actual tissue damage one way or another, perhaps they do discuss this in the full paper.

Byron Hyde writes about findings from one of John Richardson's patients that commited suicide:

Sadly no mention of any viral findings in the damaged tissue. Dr. Mowbray I believe pioneered the use of the VP1 enterovirus test so I can't imagine he wouldn't have tested these samples for virus. I'm not sure if the details of this autopsy are published anywhere, I haven't been able to find it if so.

John Richardson published the details of another one of his patients that committed suicide:

This would seem to tie together the previous two findings, but again sadly no mention of actual damage to these small blood vessels where virus was found so it's hard to say.

These findings of damage and infection of cerebral blood vessels are interesting in light of the SPECT/SPET findings of British and North American researchers, who find evidence of cerebral hypoperfusion. It's interesting to me because there are similar SPECT findings of hypoperfusion in both acute and chronic enteroviral infections of the CNS. 1 2 3

After watching Dr. Chia's recent IiME talk I see we have another ME autopsy with evidence of enteroviral involvement to add to this list. The interesting thing to me about this case is that they initially were unable to detect any viral RNA with PCR in the patient's brain samples. They had to introduce DNAse to degrade chromosomal DNA and then retest with PCR to get a positive result. This has interesting implications regarding viral persistence, underscores the potential pitfalls in viral testing in this disease, and adds further evidence for viral involvement in ME.

 

[Hip]

After watching Dr. Chia's recent IiME talk I see we have another ME autopsy with evidence of enteroviral involvement to add to this list. The interesting thing to me about this case is that they initially were unable to detect any viral RNA with PCR in the patient's brain samples. They had to introduce DNAse to degrade chromosomal DNA and then retest with PCR to get a positive result. This has interesting implications regarding viral persistence, underscores the potential pitfalls in viral testing in this disease, and adds further evidence for viral involvement in ME.

That is quite intriguing. I must send off for the IiME conference DVD and watch this talk.

Did Dr Chia say why human DNA interferes with the PCR testing of enterovirus? I know nothing about the technicalities of PCR testing, but I am wondering if this interference is a common occurrence, or whether is it something specific to enteroviruses, or perhaps specific to intracellular infections (enterovirus of course can create long-term intracellular infections).

Did Dr Chia say which cell types of the brain tested positive for enterovirus, or wasn't this determined? In one of the two previous ME/CFS brain autopsies (the Richardson autopsy), it was found that the glial cells of the brain, plus the fibroblast cells around small blood vessels of the brain, stained positive for enteroviral VPI protein.