Two corrections to your short response:

- The existence of 'wild type XMRV' is very much in question. It is exactly what are scientists are currently trying to determine. It would therefore be unscientific to use samples that are positive for XMRV according to some scientists, using unvalidated assays.

- Several studies have provided evidence for the hypothesis that XMRV is a laboratory artifact instead of a retrovirus that is actually infecting humans (1). You probably mean that these studies have not provided physical evidence that the original studies had actually contaminated their samples. That would be true (for the most part*), but science isn't 'Murder, she wrote": in science you test a hypothesis through experimental evidence. When all of your experiments support a given hypothesis, this would be considered evidence for that hypothesis. When the experiments from others support that hypothesis, the evidence could become considered to be (temporarily) conclusive by the scientific community. And the fact of the matter is that all experiments done in the Retrovirology paper support the hypothesis that XMRV is a contaminant. In other words, you wouldn't expect these results a priori if XMRV weren't a laboratory contaminant (ceteris paribus). Of course, it is always possible to later explain away evidence within any given hypothesis, which (understandably) is precisely what patients are doing on internet forums.

I would like to add that at this moment, the case 'for' XMRV nor the case 'against' it, is considered to be conclusive by the scientific community.

References

1. Robert A Smith. "Contamination of clinical specimens with MLV-encoding nucleic acids: implications for XMRV and other candidate human retroviruses". Retrovirology 2010, 7:112doi:10.1186/1742-4690-7-112. (See also the references therein)

*The fact that Sato et al (see the reference above) found that the brand of reagents that both Lo et al and Lombardi et al had used in their respective studies, is contaminated by mouse DNA, is of course some evidence for actual contamination of those studies but, in itself, not enough evidence.

Thank you for your response. The use of technical terms is not a concern to me. I was merely confused by the lack of proper grammar an spelling in your reply to me. For instance, I am not confused by the use of a "test tube" as technical term, but I wouldn't understand what a "test tune" is.

- Danielson et al have not conclusivey demonstrated what you think they have demonstrated, at least not to my knowledge. Can you please supply convincing evidence for your assertion, instead of mere conjecture?

- Like I have argued twice, you are reasoning in circles when you are arguing that some PCR assays "have a 100% failure rate in detecting viruses in people known to be infected" while others (presumably the studies you "support") "have a 100% of success". Please see my reply and example above to understand why your reasoning is circular. For further help you could also check:
http://en.wikipedia.org/w...

Thank you very much for a response that actually addresses the topic at hand.

However, I have neverv stated that 'the inability to detect something by a *different* method is conclusive proof that the original finding is false'. I and every other scientifically trained mind in the world would agree that such a statement would be incorrect. Your argument fails because it relies on the assumption above.

Like I have explained above, reproducability lies at the root of finding objective truth through the scientific method. One cannot rely on the findings of the original researchers in the way that the original commenter is proposing. The following is important to understand: this should not pose a problem at all because the original researchers also didn't have to rely on the findings of the original researchers (which would be themselves). This logically proves that any scientific experiment that is true (from that divine, omnipotent perspective you speak of), can be independently reproduced by others.

The fact that you consider your story to be equally plausible to my story (although I wouldn't agree, it may very well be), does not solve the circular problem of your story. Your methodology would only get the correct result if the original result were true, and even then perhaps because of the wrong reasons. It thus would add little if any value to the original result, just like the findings of RedLabs or VipDx add little to the argument of the original researchers.

But even beyond the above, the argument for using 'wild type XMRV' is very flawed scientifically (as I have already explained). The argument, that the "real virus" is of an "unknown level of sequence variability", does apply to the proposed 'wild type' method equally: even if a lab tested their assays against a WPI sample (or 2, or 10) of 'wild type XMRV', as you propose, it would give no more guarantees in any way that the XMRV in the 'wild' samples that they would be actually testing for their study after that, were also detectable by that assay. For what it's worth, the as of yet unpublished Blomberg study did test samples that were supplied by the WPI - I assume Blomberg was sent 'wild type' samples. Still, it didn't satisfy any proponents of a connection between XMRV and CFS: more sequence diversity was assumed and this negative study was just as quickly dismissed as the other studies.

To call the dozens of scientists that have tried to solve this puzzle to the best of their efforts "lazy"is pretty ironic considering that they have done more than you have, while asserting it may be "outright disingenuous" is against basic scientific principles.

Finally, don't forget that your accusation also applies to Alter and Lo, which also haven't replicated the original researchers' methods: surely they are also "scientifically lazy if not outright disingenuous"? I guess you would answer that they are not, merely because you happen to like their results?