Or similar endpoints we are currently unable to distinguish between.
The Undetectable Infection
- Thread starter Elph68
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Almost everyone gets Herpes viruses or Enteroviruses, so for a long time the idea was discredited, which is why the idea of pathogenic colonies of what superficially might appear to be normal bacterial species were also discredited.
Yet newer data does appear to support an enteroviral causation, and once these viruses are in play the gut will be modified, which may alter the gut bacteria anyway. The widespread pervasiveness of enteroviral infection in us, including that we appear to be the only group having anything like 83% prevalence of enteroviruses in the gut wall make this a dominant hypothesis for me.
However there may be subgroups. It also cannot be ruled out that multiple factors might make us vulnerable to enteroviruses.
In my case I am positive for Coxsackie B3 by antibody, though I have not had a gut biopsy to look for ongoing infection.
Yet newer data does appear to support an enteroviral causation, and once these viruses are in play the gut will be modified, which may alter the gut bacteria anyway. The widespread pervasiveness of enteroviral infection in us, including that we appear to be the only group having anything like 83% prevalence of enteroviruses in the gut wall make this a dominant hypothesis for me.
However there may be subgroups. It also cannot be ruled out that multiple factors might make us vulnerable to enteroviruses.
In my case I am positive for Coxsackie B3 by antibody, though I have not had a gut biopsy to look for ongoing infection.
Exactly my thoughts. I posted a study earlier showing a particular virus in the lungs increased substantially bacterial colononization.
Just sent my 2nd biopsy in to Dr Chia and eagerly awaiting my results.
Just sent my 2nd biopsy in to Dr Chia and eagerly awaiting my results.
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I will PM you in the weekend. 
I know that many researchers say that since most people who catch herpes family viruses and enteroviruses and remain healthy, these viruses cannot be the cause of ME/CFS. But that argument is complete nonsense.
If you look at poliovirus, for example: when poliovirus was still in circulation, most people catching this virus would show no symptoms at all, and remain totally health and unaffected by it. However, a tiny percentage of people would develop poliomyelitis after catching poliovirus — sometimes with fatal consequences.
Thus the idea that because a virus causes no symptoms in most people, it therefore cannot cause some disease in a minority of individuals is a totally incorrect idea, as the poliovirus case demonstrates. I cannot understand how any researcher can even suggest such an idea.
If you look at poliovirus, for example: when poliovirus was still in circulation, most people catching this virus would show no symptoms at all, and remain totally health and unaffected by it. However, a tiny percentage of people would develop poliomyelitis after catching poliovirus — sometimes with fatal consequences.
Thus the idea that because a virus causes no symptoms in most people, it therefore cannot cause some disease in a minority of individuals is a totally incorrect idea, as the poliovirus case demonstrates. I cannot understand how any researcher can even suggest such an idea.
I should point out that it is very easy, just using simple logic, to prove that herpes family viruses such as HHV-6 and EBV cannot be the triggering viruses of ME/CFS. This logic is as follows:
You can exclude herpes family viruses from being the precipitating infectious cause of ME/CFS simply by the fact that (a) ME/CFS most frequently develops in adults, (b) nearly all adults will already have HHV-6 and EBV in their body, since HHV-6 is usually picked up before you are 3 years old, and EBV is picked up usually in the teenage years. Ergo, when you observe that you have caught some virus that then precipitated your ME/CFS, it is very unlikely to ever be HHV-6 and EBV, since the majority of adults already have these two viruses in their body already.
I am not sure why ME/CFS researchers have overlooked this basic fact, which generally rules out HHV-6 and EBV as being the triggering viruses of ME/CFS. Of course, HHV-6 and EBV already in your body may be reactivated by the immunosuppression of ME/CFS, and may then contribute to ME/CFS symptoms, sure, that is another story. So it is still a good idea to take anti-herpes drugs. But HHV-6 and EBV cannot be the triggering virus of ME/CFS that you catch as a adult, in the general case at least).
Enteroviruses such as coxsackievirus B and echovirus are a different story, because although one or two of these may be caught early in life, there are in fact 6 serotypes of coxsackievirus B (not to mention the various sub-strains of each serotype), and there are 32 echovirus serotypes, so you can certainly catch a nasty enterovirus later in life as an adult, even if you caught one as a child.
You can exclude herpes family viruses from being the precipitating infectious cause of ME/CFS simply by the fact that (a) ME/CFS most frequently develops in adults, (b) nearly all adults will already have HHV-6 and EBV in their body, since HHV-6 is usually picked up before you are 3 years old, and EBV is picked up usually in the teenage years. Ergo, when you observe that you have caught some virus that then precipitated your ME/CFS, it is very unlikely to ever be HHV-6 and EBV, since the majority of adults already have these two viruses in their body already.
I am not sure why ME/CFS researchers have overlooked this basic fact, which generally rules out HHV-6 and EBV as being the triggering viruses of ME/CFS. Of course, HHV-6 and EBV already in your body may be reactivated by the immunosuppression of ME/CFS, and may then contribute to ME/CFS symptoms, sure, that is another story. So it is still a good idea to take anti-herpes drugs. But HHV-6 and EBV cannot be the triggering virus of ME/CFS that you catch as a adult, in the general case at least).
Enteroviruses such as coxsackievirus B and echovirus are a different story, because although one or two of these may be caught early in life, there are in fact 6 serotypes of coxsackievirus B (not to mention the various sub-strains of each serotype), and there are 32 echovirus serotypes, so you can certainly catch a nasty enterovirus later in life as an adult, even if you caught one as a child.
Yes, I agree Hip that common pathogens that everyone gets can indeed be a cause, yet the CDC was pushing this for a very long time if I recall correctly. It also ignores what we know of immune response - how respond may alter the outcome. In some diseases there is a discreet difference in outcome based on patient response. I think Leishmania is one.
Herpes virus cannot be ruled out for similar reasons that enteroviruses cannot be ruled out. These viruses lurk, and the damage may be a result of widespread neurological infection, and that takes time. Then something comes along and triggers the disorder. However I find the Herpes virus argument much less compelling than the enteroviral one.
I do agree that most Herpes infections do not make sense as a triggering virus.
Herpes virus cannot be ruled out for similar reasons that enteroviruses cannot be ruled out. These viruses lurk, and the damage may be a result of widespread neurological infection, and that takes time. Then something comes along and triggers the disorder. However I find the Herpes virus argument much less compelling than the enteroviral one.
I do agree that most Herpes infections do not make sense as a triggering virus.
I think this is why the cfs gurus are now looking more into the immune syste. Can't remember who said it but they use to call cfs The Bug of the Month. So many different infections were implicated but they couldn't nail it down to one cause.
I think it was dr Nicholson who said the longer one is sick with cfs the more infections they find.
Many cfsers can remember the onset of cfs, maybe this initial infection is what has 'broken' the immune system, which then leaves us open to other infections. The immune dysfunction especially nk function seems to be the most common finding more so then anyone infection.
Hopefully in the next 12months we have more answers from researchers. Promising thing is we seem to have more researchers than we have had in a long time.
I think it was dr Nicholson who said the longer one is sick with cfs the more infections they find.
Many cfsers can remember the onset of cfs, maybe this initial infection is what has 'broken' the immune system, which then leaves us open to other infections. The immune dysfunction especially nk function seems to be the most common finding more so then anyone infection.
Hopefully in the next 12months we have more answers from researchers. Promising thing is we seem to have more researchers than we have had in a long time.
It's not impossible for ebv cmv hhv6 to be the initial trigger, maybe more common then your indicating. I say this as the dubbo studies followed people (adults)after glandular fever infections as well as other viruses. It was about 10% who ended up with ongoing fatigue. Cmv mono that was apart of my cfs onset at the age of 31. Again I think it's a sub group thing and whenever cfs is researched there's always this ebv group that pop up. Dr Peterson has mentioned that this herpes sub group are the group that they can potentially improve or maybe cure as there's treatments available.
We are just all unique with infections and immune issues but all have cfs me. When they eventually work this mess out, I think we are all going to need different treatments. It would make it easier if there was just one universal cause
We are just all unique with infections and immune issues but all have cfs me. When they eventually work this mess out, I think we are all going to need different treatments. It would make it easier if there was just one universal cause
Or mycoplasma or ebv or enterovirus. The list is long.
Tell us more about availability of testing and accuracy. Is it a biopsy only test?
Tell us more about availability of testing and accuracy. Is it a biopsy only test?
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Taking an immunemodulator.
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I do not want to. I am satisfied with the symbiosis.
and why the monoclonal antibody rituximab produces remission in a good proportion of sufferers.
I am bemused that you think that you know better than numerous eminent scientists, and better than the scientists among us who have read, and evaluated, and made connections between many many scientific findings.
I'm not saying that your theory is wrong, just that your level of certainty appears excessive.
I am bemused that you think that you know better than numerous eminent scientists, and better than the scientists among us who have read, and evaluated, and made connections between many many scientific findings.
I'm not saying that your theory is wrong, just that your level of certainty appears excessive.
I have never heard cytokines being called enzymes before.
I certainly subscribe to the theory of compromised biological barriers allowing pathogens access to the bloodstream and hence the whole body. My own preferred theory is that this leads to autoimmunity, as described in this paper.
Microorganisms are well-known to mutate, so the theory of symbionts becoming pathogenic is plausible. However, I believe that it is more normal for microorganisms to become less pathogenic or non-pathogenic after inhabiting a living body for some time, unless perhaps there is gene transfer to them from a pathogen. It is not in their interests to start causing damage to their hosts after living in harmony for so long, as it could reduce their own chances of survival.
Is gene transfer part of your theorised mechanism?
I certainly subscribe to the theory of compromised biological barriers allowing pathogens access to the bloodstream and hence the whole body. My own preferred theory is that this leads to autoimmunity, as described in this paper.
Microorganisms are well-known to mutate, so the theory of symbionts becoming pathogenic is plausible. However, I believe that it is more normal for microorganisms to become less pathogenic or non-pathogenic after inhabiting a living body for some time, unless perhaps there is gene transfer to them from a pathogen. It is not in their interests to start causing damage to their hosts after living in harmony for so long, as it could reduce their own chances of survival.
Is gene transfer part of your theorised mechanism?
I can't think what might be unsuitable for under-18s to read about a medical issue, considering what else they can view on the internet!
In that case I would not call it an STI, but an infection transmissible between people.
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Right