Well, I guess we disagree then, because I think blood-borne retrovirus by definition is a disease transferred by sexual contact, sharing needles by intravenous drug users, or vertical transmission (mother to child from breast milk generally). That is a very well-known epidemiology for HIV and HTLV, as well as a host of animal retrovirus diseases including MLVs and probably other gamma forms. ME/CFS on the other hand occurs in outbreaks among large, definitely non-conjugal, populations, within a short timeframe, such as during a flu-like illness outbreak. ME/CFS also occurs randomly in smaller clusters, in families, or in individuals. Long-term sexual partners of ME/CFS patients do sometimes get sick as well, but more often do not. A small but stable percent of post-viral patients go on to develop ME/CFS after EBV, parvo, Lyme, and probably others. I believe this puts ME/CFS in a category of genetic precondition plus air-borne or water-borne trigger pathogens.
Yes, you have said before that the retrovirus may have become universal through some unknown mechanism, such as vaccine contamination, and that we might just have unlucky genetics. That would be consistent with genetic precondition plus post-viral infection. But that theory has an up-hill battle because there have been outbreaks of ME/CFS since ancient times, by many accounts. Most recently during the Crimean war, the US Civil War, WW I, in the 1930s, the 1950s, and the 1980s. In the case of XMRV, that virus may be a lab creation from the 1990s, so unless it is a time-traveller, or the virology field has this all wrong, I think this idea would be a fringe theory. That said, sometimes fringe theories turn out correct, but I think in this case it is long odds.
Of course there might also be a novel transmission mechanism, but that would be huge if true, as it would apply to a host of retroviruses, and I have not heard any real evidence for that idea, just postulate. In fact there have been searches for novel transmission methods, I remember reading a study of ticks and retrovirus transmission a few years ago, I believe conducted in Africa to see if HIV spread by ticks, but if my memory serves there were enzymes in ticks that de-activated the retrovirus.
Hi Kurt, in 1955 it was shown ME is blood transmissable here in Australia although I have yet to get hold of the paper - I think it involved finding the same lesions in the brain and spine of monkeys some time after infusion. It was quoted several times after that. We also know many patients get sick after blood transfusions - around 5%. A retrovirus can not only cause similar pathology to that found in ME and CFS, it has a slow incubation period. MLLVs are likely to have a much slower incubation period than HIV, and it can take 20 years for someone to get AIDS (not usually perhaps, but its known). Every person could have contracted the retrovirus long before an epidemic, the epidemic was simply a confluence of factors that combined to trigger a retroviral outbreak in people already infected. The incubation period thus matches the coinfection that triggered the retrovirus. The retrovirus could even be passed down generation after generation, awaiting a trigger. Its spread in the population is likely to be a patchwork, not ubiquitous.
MLLVs have been around for many millions of years. Thats
way longer than the known or suspected history of ME and CFS. They infect many different vertebrates, from birds to gibbons, cats and koalas. Humans would have come into contact with them millions of times, if not billions of times. We have very strong antiretroviral defences against them .... why have we such strong defences? The most plausible explanation is that we have been infected before, and it was devastating, causing a huge evolutionary advance in
resistance (not immunity). Is every outbreak of ME or CFS is the same retrovirus? There are many strains of MLLVs out there. It is also possible that some, most or all outbreaks are not MLLVs at all, it could be another retrovirus.
The claim that XMRV arose as a lab recombination event in the early 90s is an hypothesis, several studies found it or something like it in the 80s that have been commented on since several times. This hypothesis is accepted far too readily. Even if its correct that recombination created the virus in the lab, pure chance (as I have discussed repeatedly elsewhere) could have created it millions of times in the natural population last century alone. So what if it appeared in a lab culture? They also did not rule out that the virus
contaminated the culture. It does that, quite readily as it turns out. If the virus was around, it had a much higher probability of contaminating the culture than a chance recombination event. The recombination event is actually a much more unlikely hypothesis. Please note that I am not saying I know they are wrong, only that we should be sceptical.
The Lipkin study is the final world on XMRV-like MLV association as far as I am concerned. We wont know to a high degree of certainty until then. Even then it does not rule out the existence of an entirely different retrovirus, or even endogenous retrovirus reactivation via some mechanism. Nagalase is often found in patients, and it can come from a retroviral infection, though thats not the only cause. I think there were reports of isolated findings of reverse transcriptase, but I don't think its ever been systematically followed up. If it was followed up an d showed very high prevalence of reverse transcriptase in patients, it would clinch it in my view. We know of no other cause for reverse transcriptase.
I am not saying my model discussed here is correct, only that it fits the facts. I am still completely open to an autoimmune/regulatory problem as the cause, it was where I started in the 90s and it still makes sense. The Rituximab study unfortunately could be either immune or viral, as B cells can be affected by viruses, retroviruses or defects in immune regulation. It could even be due to an unintended side effect of Rituximab, not the B cell depletion at all. This is early days in the research.
To me one of the great questions is: why is there such a high viral tissue load, especially in the gut (but also muscle, including heart muscle)? What causes this? When we know the answer to that, I think we may be close to cracking the origins of ME and CFS. One of my hypotheses, a variant of something I said years ago, about low NK cell function is that it may be deliberate. At some point with a high viral load the body might have started attacking gut or heart, and the immune system was suppressed automatically. in other words, its a survival mechanism. Against this we of course have the issue that some patients with low NK cell cytotoxicity (and lets not forget T cell cytotoxicity is down too) have had the cytotoxicity restored and have not dropped dead, so I am not completely happy with this hypothesis.
The data is looking more and more like there are at least two types of CFS or ME. It is also possible this is subgroups due to genetics or some other factor. I would be interested to know if patients selected from specific outbreaks did not exhibit such subgroups.
Bye
Alex