Lipkin's notion that his study will conclude the science is both unscientific and perversely dangerous. It is a statement that can only be made after the fact, and pertaining to
aspects of his study that provide
reproducible explanations for discrepancies.
I really hope that the WPI has a very concrete grasp of the precise mechanisms driving the postive/negative differences (as Judy alluded to by saying they thought processing was key). Without this trump card up their sleeve, I can very easily see the WPI being quietly swept aside behind the scenes in a landslide of ignorance and bias.
As for odds, I would say 95% in favor of (co-)causation. At the end of the day, the two positive studies are still very strong and indicate strong association between HGRV and CFS. The WPI demonstrated that XMRV is both infectious (and produces an immune response) and not endogenous (via sequencing and blasting). Both studies taken together provide strong evidence of a genetically diverse infectious human retrovirus. Both studies also went to great lengths to rule out contamination. Additionally, the pathogenetic model of retroviral infection in humans (and MLV infection in animals) fits CFS like a glove.
The only countervailing evidence is a set of 0/0 studies that prove nothing more than their collective inability to find the virus. Not one of them provides any explanatory evidence that either positive study is a "false positive." Thus far, the only hypothesis proffered as potential explanation for "false postives" is contamination. And this hypothesis has vastly more evidence stacked against it (checks/controls in both postive studies; vastly higher percentage found in CFS than controls, consistent across positive studies; antibody response; genetic diversity of strains found, suggesting true infectivity; Coffin's failure to find XMRV in any of 70 species of mice,
i.e. from whence doth thy contamination spring) than for it (is there any evidence beyond "well, we've arbitrarily chalked up similar discrepancies in the past to contamination"?).
Researchers have no reason to try and not find something, everyone wants to be the first one to replicate the results.
This seems to be the overarching theme repeated
ad nauseam on this forum, despite the fact that there is a surfeit of historical evidence (regarding both CFS and other diseases) against this rosy notion. Furthermore, how can you logically claim "everyone wants to be the first one to replicate the results" when absolutely nobody (except the Alter study) has even
attempted a replication study? Can someone who, at the crack of the starting gun, wanders into the infield to sit and play with dandelions really be accused of "wanting to win the race"?
I also know that while science (and certainly the politics surrounding it) can move painfully slowly, and that we have paid a terrible price for that, I still would much prefer they took a little longer and got the answer on XMRV right.
Actually, I think things are moving at a reasonable pace, considering what is at stake. This issue goes way past ME/CFS patients, it is potentially one of the most serious disease factors in human history. For everybody's sake, including ours, we must allow the basic science of XMRV (et al) to be firmly established. We must be able to clearly define and detect the relevant organism(s), before we can do anything else, including serious clinical trials.
I agree that being careful and thorough is important. I think, though, that much of the frustration with the pace of research is very legitimately derived from an obvious lack of haste and funding from the relevant government agencies. Why did it take a full year to form and fund operations like the BWG and Lipkin study? It took no time for the CDC to fire off a shoddy 0/0 study, yet a full year later even modest research funds are not forthcoming to the WPI and other, dare I say, competent researchers. That is not being careful. This is being deliberately slow.