Hi fellow travellers,
I thought I would post my current interpretation on a big picture, then make some random comments. Much of what I am going to say has been said already on this forum, but it is worth putting together. I am not going to mention who said what as they are so many of you - which is a good thing!
This is my current model of XMRV and ME or CFS. It is only one possible model, and I don't presume it is correct.
The XMRV infected population is perhaps 6%. I have been saying this for months now, but the figure depends on the data used, I get anything from 1.7% up to 9.72%, and my most recent calculation was 5.1%. What is missing from the oft quoted 3.7% is that this is the HEALTHY people. Add in the percentage of sick people (which goes up as the number of diseases it is found in increases, and goes up or down with the latest coprevalence figures). This gives you a true picture.
The suggestion of 10% is not impossible. The Dubbo study showed that around 10% of patients with a severe infection develop CFS. We are also ignoring the very large numbers of patients with post-transplant fatigue and post-cancer fatigue. Fatigue is the NORM in these disorders, and many never recover. Spend some time on the postcancer fatigue forums and you will see that the description is almost identical to CFS, it is just that having had cancer a CFS diagnosis is excluded. These patients have yet to be tested for XMRV (except of course for some prostate cancer patients).
The CFS population is a highly overlapping subset of the XMRV population, but it may not completely overlap. The same is true of the other disorders that are implicated - atypical MS, autism, FMS, GWS etcetera, which may also overlap with each other.
Let me ask a question: if 3 to 6% of the population have XMRV, then what happens during a viral epidemic? Perhaps everyone who has XMRV and a severe infection gets CFS. This is the two hit hypothesis, which I proposed many years ago but nobody was interested at the time (but is popular now that we know about XMRV). It seems to me that first you get XMRV, and then something triggers it - it has androgen and cortisol sensors for a reason! The KIND of trigger determines whether you get CFS or FMS or both, and so on for the other disorders including autism. Genetics probably does play a role, but all of these disorders will have to be examined to look for genetic links with XMRV. From the Incline Village epidemic experience, it has been claimed that it is unlikely that XMRV could cause CFS due to the XMRV incubation period (10 to 21 days). The epidemics simply spread too fast. However, if the two hit hypothesis is adopted, then this problem disappears. The epidemics are just conventional diseases that trigger the underlying XMRV infection and so result in CFS.
(Does anyone know if FMS trigger points correspond to lymph nodes?)
Peterson has commented that he has found that "recovered" CFS patients are not doing well. This is extreme speculation, but it is possible that they suppressed the CFS reaction from XMRV but not the virus - and this has long term consequences. Curing CFS without removing the cause is only a temporary solution.
This would make XMRV cocausal, not a sole cause. It would however also mean that XMRV is a necessary requirement for getting CFS, and result in the kinds of percentages we are seeing, as well as explain both slow (repeated immune insults) and sudden onset CFS (severe immune insult). It would also mean that if you suppress the XMRV completely, you could halt CFS progression, and if you can elimate the viral host cells you can cure CFS (ignoring the problem of genome integration). Of course if something like the Peroxnitrite Hypothesis (Martin Pall's work) is correct, then treating XMRV is only the first step - you still have to shut down the CFS response.
Now, there is the alternative explanation, that we have the same risk of contacting XMRV but are particularly susceptible. I think this is unlikely, as unless we have a VERY specific immune abnormality (eg low NK function, or genetic predisposition) that gives XMRV a serious edge, you should find nearly every transplant patient has the same prevalence of XMRV as they are all susceptible. You should also find a very high prevalence of XMRV in HIV patients. We will see, but this doesn't look likely. It would also not explain the epidemics, unless the specific immune weakness allows for very much shorter incubation periods.
And now for some random comments, all relating to one post or another on this thread:
Lynn (tloyd) is right - if it can be shown that XMRV is pathogenic, we can all be treated even without proof of XMRV causing CFS, as long as we are XMRV positive. The worry is that not all of us will be.
It was noted somewhere on this thread that early studies on prevalence of CFS showed that some professions are more likely to get it. I would like to repeat and expand that list: medical professionals (not just nurses or doctors), teachers, airline pilots, serious endurance cyclists. All of these people have major exposure to viruses, and the cyclists are at risk for overtraining which suppresses the immune system.
I was at a conference in 1999 when de Meirleir discussed the risk of CFS being blood transmissable. For most of the last decade this was ignored. Haemopheliacs are very aware of the risks, just spend some time on their forums. The news that blood products can have XMRV inactivated is very very welcome, and may be a better solution than testing for the virus, although both approaches together would be much better.
I have been worried for months that the combination of XMRV in saliva plus high stability might mean this virus is airborne. I have held back on public forums because I didn't want to cause public panic, and in particular because many with CFS have close family members and the worry could seriously degrade their health - and we don't know for sure yet that it is transmissable this way. In fact, we only know that it can be transmitted by blood contact, everything else is speculation. However, it is looking more and more like XMRV may indeed be airborne, although another possibility occurs to me. XMRV appears to replicate when there is another virus present, or some other immune challenge (injury, poisoning etc). What better place to wait than in the lungs, given how many respiratory infections are floating around?
XMRV has a very very low viral load in the blood, and I suspect the same in the sputum and saliva. It could easily be airborne, but the transmission rate could still be very low. This is because the virus will often die quickly (even if it is stable, the low load will mean there is very little virus present and so is at higher risk of all of it dying). Think of this as a half life - the total number of virus particles halves every so many minutes. XMRV would have a much longer half life than HIV (which has a very short half life, it dies quickly after leaving the blood), but with so few virus particles present it wouldn't take long for all of them to die. The real risk then would be the omniprevalence. With maybe 5% (or pick another number) of the population spreading it all the time, then it will slowly spread to anyone who can't fight it off, then lurk waiting for a trigger. I think Mary Schweitzer said it best, although I may be misquoting her (I don't remember very well): XMRV is to CFS as HIV is to AIDS. Not everyone with HIV gets AIDS immediately, it lurks. There is no reason to suspect that XMRV is any different, and given its low replication rate it probably lurks for much longer than HIV does. If XMRV is airborne, then Humanity is very very lucky it is not very transmissable or we would all have it. Of course if we ignore XMRV then that could still happen, it would just take longer.
I would like to thank Cort for Phoenix Rising and these forums: these have become my first stop after reading my email. Good work.
Bye
Alex Young
