Thanks. Unfortunately i don't have an office suite installed on this computer and i have to leave in 30 minutes, so i can't look at it.
It seems they studied some forms of cancer, not CFS, but still it sounds very interesting.
Great to see that Mikovits, Lombardi and team are pushing things forward and creating facts while others just talk and wonder if there really is something. As soon as i can, i will make another donation to the WPI.
Not being medically trained, I cannot figure out what this document means. I converted it to a PDF file. Hopefully someone else can interpret the data into layman's language. View attachment Snyderman_XMRV-1..pdf
I got this message when I clicked on the original link:
"This file is no longer available.
The file you are looking for is no longer being shared at this address. The link has either expired or the owner of the account has decided to stop sharing the file. If you still need to access this file, please contact the owner of this MobileMe account."
BW...it isnt the first time those cancers have been linked. they suspected it for years.
this is proof ARV's lower viral load.
perhaps i should not have been so hung up on latent proviral load problem...the virus produces "chronic replicative" infection in those monkeys so perhaps ARV's will be the way to go. maybe the slower recovery speed (as compared with HIV) has to do with the fact that the virus just replicates slower?? i dont know...
Here's what I posted in the comments there on why JDJ might have referred to this "little" poster as "historically important."
"There are many historically important things about this study, but the ones that are pretty mind-blowing in my view:
1. That XMRV could be both detected in these cancerous cells and generated (expressed) from cell cultures made from these cells makes for a strong association between the virus and the diseases.
2. That antiretroviral therapy lowers not only cytokine markers for XMRV, as one might expect, but actually lowers markers for the tumors themselves... along with clinical improvements, strengthens the potential causal association.
3. #2 is just mind-boggling because it suggests that the cancerous conditions are being driven or maintained by the continuous presence of the virus, rather than that the virus turns on the genes for the cancer (or off genes that prevent it) and then its presence or absence has no effect.
Think of it this way- you could treat these cancers by antiretrovirals rather than chemo, radiation or surgery.
Or another way- maybe cancer is the result not the problem.
This is big stuff if it bears out in larger groups.
Besides all that, there is that little thing of those folks who are XMRV positive being able to prevent potential cancer... "
In addition, the poster reveals some of the cytokine markers Mikovits has been using for XMRV. I haven't had time to look at these, but some of the smarter forum posters may be able to tell us more about these.
Thanks for explaining all that JimK, I too was struggling to make sense of it. I don't understand cancer well enough to properly understand why the finding seems so bizarre, but I do know that smart people regard "bizarre" anomalies as potentially important, even revolutionary, and the source of significant new scientific knowledge...whereas the conservative mindset regards "bizarre" findings as things to be automatically dismissed as "impossible". I've felt for a long time that XMRV could turn out to be one of the most important scientific discoveries for decades, and every result like this just strengthens that sense. Really exciting stuff!
OK so I've just done a bit of reading to try to understand this point. First impression of a self-confessed amateur is: Isn't it more accurate to say that tumors are driven by errors in the process of mitosis? The cell division goes wrong. So the implication of these results would then be: XMRV can cause errors in the mytosis of certain types of cells? Remove the XMRV, and the mytosis stops going wrong? Could XMRV do that directly, or could it alternatively suppress some natural mechanism for correcting faulty mytosis? Final thought: being a gammaretrovirus, the size of XMRV seems significant and it could potentially be "packaged" by other cells. So if it were able to get inside certain types of cells, could that cause the mytosis to fail? All seems to make reasonable sense to me...but perhaps that's because I don't really understand it...