The amplification processes and activation are the issue kurt I,m genuinely sorry that you dont appear to be able to grasp that .You would not find a latent virus using PCR without that.The rest is speculation without any fact to back it up.The issue about herv activation is not an issue it has been dealt with by experts and put to bed. The issue with PCR is false negatives and that is why it is not considered reliable enough to confirm or more importantly dismiss a hiv infection.
Yes, real-time PCR can produce false negatives, that might have been a problem with the UK and Dutch studies. But standard PCR can produce false positives, and the WPI might also have that problem. Validation by outside studies with a valid cohort would help illuminate that issue.
HERV activation was not seriously dealt with in the Science article and it remains a significant possible confound for the antibody and culture portions of the WPI study given the cross-reactivity of MuLV antibodies. WPI does not have any XMRV antibodies, nobody has discovered them yet, at least that is reported.
If CFS samples have HERV activation, then if a viral protein is activating those HERVs it would likely be in the blood fraction used in the transfection. And since WPI was infecting prostate cancer cell lines, it seems very possible that the viral protein then also transferred over, activating the same HERVs in the prostate cell line. Then in the final step, the MuLV antibodies might get hits on the activated HERVs in the new cell line. I am not claiming this happened, just pointing out that there is an alternative explanation that must be ruled out.
If , would be likely it seems very possible might science does not deal with speculation kurt but objective observations.If any of this had been observed then it would of course have to be accounted for. If it is mere speculation however it is irrelevant
Speculation? What was observed during the WPI transfection study could be explained by other than the proposed hypothesis that they saw XMRV infecting new cells. WPI has hypothesized that their process proves XMRV is infecting, but they have not to my knowledge ruled out the alternative hypothesis that they created HERV activation transfer. Their final antibody test also does not rule out HERVs, in fact MuLV antibody is one possible test for HERV activation. All that was objectively observed was that at the end of the transfection process the MuLV antibodies got hits.
I am very suprised that you are not suspicious of 3 studies rushed out in 51 days by psychiatrists who's carreers are heavily dependant on portraying CFS as a psychological illness
I don't have a suspicion like you might have in the UK of the motives of those researchers, but I do understand why you would be suspicious. I am FAR more suspicious of activities and claims of private companies like VIP/WPI, given how things often work here in the US. But yes, those tests were rushed, I agree that is a risk, they ran convenient samples using existing PCR techniques readily available. This rushing does not by itself prove anything, but it casts doubt. And suggests that they do not value the CFS population enough to run a fresh study using carefully designed testing procedures and new samples from a strong cohort. Sad state of affairs.
The cohort of the Dutch study certain is questionable as you pointed out in another thread, which is too bad because that was probably the strongest assay yet in a follow-on study. So at this point my only conclusion about those 3 rushed studies would be that they are weak, and certainly insufficient evidence to draw any global conclusions. I hope we get better studies by summer. Anyway, I don't need to do the dirt digging there, others here already have.
There is still a possibility that the tested cohorts in those three studies simply had no XMRV. We really need to see some stronger studies though to get a better sense of how widespread the virus really is. IF XMRV is a false finding for CFS, then whether or not the UK and Dutch studies were adequate will become a moot point.
I am not clear one one point however did you say you were a psychology graduate or didn't you
I look forward to your new and powerful information
Yes I graduated, my field was an integrated discipline similar to what you might call I/O psychology (industrial/organizational), although mine was a Systems focused program, more technology. So that included psychology, technology and systems, educational/training research methods, things like that. Then worked for a few years as a research psychologist, a post-doc at a US military research lab. Then later worked as a systems designer for MD training project (Cardiology), then worked for a private military research company, where CFS totally wrecked my career. Anyway all that really transfers from that experience to CFS is that I learned how to read research, and having authored studies and been a peer reviewer I realize the limitations of published research reports.
So you said you had a degree in chem/medical, were you a microbiologist, a lab technologist or med tech?
New and powerful information ... would be nice. I believe that can come from connecting all the many pieces of the puzzle we have now in front of us. The role of HHV, HERV K18, enterovirus, other co-infections, glutathione depletion, methylation problems with SNP expression, mitochondria malfunction, cytokines, NK problems, pain/fatigue receptor over-expression (PEM), and problems from resulting neuroendocrine over-stimulation all need to be connected together. What could cause all of these to express together as they do in CFS? That is a theory I would like to see, using a systems biology approach. I have talked with other researchers, including biomedical, but have found nothing concrete, no workable systems model that could include all this. Maybe all these clues ARE the model for CFS, who knows.