Sorry if I'm missing some things – had to take a break due to health.
A possible explanation for the above contradiction: the answer may relate to the fact that the ARUP lab tests John Chia uses are capable of detecting and measuring individual titer levels for each of the 6 Coxsackie B virus serotypes, whereas in the 1991 paper, their IgG test just measured the overall coxsackievirus B titers in general; it was not able to distinguish individual serotypes.
I don't know about the intricacies of antibody testing, but possibly this might mean you get an averaging effect in the 1991 study IgG test, which might blur any individual high titers found in any particular coxsackievirus B serotype.
This is a good possible explanation. Some labs are total crap. See for example Labcorp. I have apparently been exposed to every Coxsackie B virus any many types of A (this is 2014):
Quest labs (2013) is similarly confused:
ARUP, however, thinks that I ONLY have only been previously exposed to Coxsackie B4, as opposed to nearly every type of Coxsackie virus:
2016:
2016:
Now obviously, researchers have access to even better tests, but the testing used varies widely from paper to paper and it
MATTERS. A lot.
Some of the best researchers in the world, notably Dr Lipkin (the virus hunter) and dr Davis looked for signs of infection and did not find it. It is truly painful to return over and over to past theories which haven’t gained much momentum except for 2 physicians, one of whom sells his own compound to treat it (and it’s not cheap) and the other one who collects a lot of money from patients in the context of a socialized health care system..
I think
@Hip already answered this but with current methods, you aren't going to find latent virus in tissues when you are looking in the blood. This may change. When we look in places other than the blood, we
DO find direct evidence of viral RNA in a subset of patients.
It has nothing to do with being the best researcher in the world. They're just not looking at tissue samples.
None of this addresses the direct evidence. We should also be careful re: ad hominem arguments. Chia is so not in this for himself. He is one of the only doctors who actually, truly takes insurance. And frequently, he doesn't treat the people he diagnoses. He may try Equilibrant as it does seem to help some people (and did help me earlier in my illness), but there are loads of treatments I ask him about and he says "yeah, that didn't work so I don't try it anymore" or "1/3 or 50% got better but everyone relapsed after treatment." He is also down on experimental treatments that may be expensive but not covered by insurance as he doesn't think the evidence it there to justify either the risk or the cost. I find him to stick very closely to his observations. I expect he thinks we need anti-enteroviral drugs to truly deliver benefit to most patients.
I don't know. But Ron is saying that he's trying to develop a probe for RNA in the blood now (but expects it to be difficult because RNA is unstable).
That's great. This is very important.
Thanks for the explanation,
@Hip. Do you have any links for research that provides evidence of this being present in ME/CFS?
Here is another citation Trish:
http://me-pedia.org/wiki/Coxsackie_B_virus#Chronic_infection Mechanism seems to be change in ratio of positive to negative sense RNA. I believe there are other studies that find this general phenomenon (say, in mouse models of Coxsackie myocarditis) but I haven't finished pulling in all the citations into the Coxsackie B page. Many are on the discussion page:
http://me-pedia.org/wiki/Talk:Coxsackie_B_virus But chronic infection is well studied in animal models and is
not normal in the way that we consider chronic herpesvirus infection to be normal.
This is also interesting and I think a direct affirmation of what Jane Colby has said, which is that early in a Coxsackie infection, rest is extremely important:
http://me-pedia.org/wiki/Coxsackie_B_virus#Exercise
Enteroviruses are all but harmless and have been linked with type 1 diabetes (
paper), chronic myocarditis, the 2014 EV68 and other outbreaks where children have died, etc.
I'm not sure what you mean by all but harmless. They are the most common cause of aseptic meningitis for example (85-90% of cases). Polio was harmless to the vast majority of people who contracted it (usually asymptomatically). The harm was in the tails, but it was on a scale large enough that people felt it was important. Re: myocarditis, I don't think there's good evidence this is a downstream effect. All animal evidence points to a direct effect of inflammation of the heart due to acute (or chronic) infection.
Due to all these enterovirus caused health issues, especially the recent EV68 outbreak, I'm hopeful that enterovirus drug development will be accelerated and that an effective drug against enteroviruses will reach the market in the next few years. In Finland there is now a
vaccine in development against enterovirus in order to prevent or at least reduce likelihood of developing type 1 diabetes. This vaccine has been successfully tested on mice and they are looking to start a human trial by the end of this year. And then as was mentioned there are the two Belgian drugs being developed. Response to these drugs could finally shed some light on whether enterovirus on its own can cause and/or maintain ME/CFS.
This is all wonderful and absolutely.
