At the end of the day, we would ask only one thing of the researchers: to prove that the XMRV virus CAUSES CFS symptoms (i.e., meets Koch’s postulates).

Typically, that causation would be first shown in animals. However, no established animal model of CFS exists. So, without an animal model to show causality, the only option we have is to establish a link (i.e., a correlation) using epidemiological studies in CFS patients, which are statistically driven and only as robust as their numbers. (Mikovits has admitted this problem publicly in interviews. See, for example, http://www.nature.com/scibx/journal/v2/n40/full/scibx.2009.1492.html )

Thus, the best we can do is show a correlation between frequency of the XMRV DNA sequence in patients and frequency of CFS clinical symptoms – and, so far, when we look at all the epidemiological studies published on XMRV and CFS (not only the Mikovits study), that correlation is looking very week – and we’re not even talking about cause here, which is the gold-standard in infectious disease.

Laboratory contamination may or not have happened – and that issue should be sorted out – but even if it didn’t happen, these findings are still only correlative and not something anyone would want to base any kind of treatment on.

Bottom-line: scientists cannot allow desperate patients to influence the way they carry out and report research. I’m very sorry if that sounds insensitive, but it’s for the best of both the scientific community and patient groups.

Mr. Dick Turpin

I believe that the Whittemore’s found Dr. Mikovitz at NCI. Whittemore’s reason to research the disease is that their daughter has a severe case. This isn’t a $$$+ venture for them, they already knew how to do that. But no matter how much $$$$ they couldn’t restore their daughter’s health.

Add into the soup that some specialists charge upwards of $6K for an initial visit & compare that to the $500 test.

@ Michael Not one of the groups coming out with negative results has done a replication. One group came out a non-replication within 6 mos of the Science article having not found the virus, a laughably short time. Another non-replicator admitted to Dr Mikovits leaving out a step that Mikovitz felt was crucial, and hasn’t tried again. A third non-replicator had the astounding foresight to say that he didn’t think that he would find the XMRV -CDC’s William Reeves. There was a paper by Lo& Alter(FDA & NIH)which confirmed WPI’s findings. That paper was held back for more than a month to retest after CDC came up empty handed. So it’s high time that a replication study was undertaken. As there are some 800,000 people in the US suffering from this unimaginably debilitating & contagious (See Lyndonville, Royal Free Disease,..others)illness, it’s about time that serious study be undertaken. It’s not a new disease but a rediscovered one. It keeps getting rediscovered (and renamed) every generation or so after it’s been forgotten by yet another generation of doctors

There is a great deal of speculation that could be resolved by doing some basic research on Google.

No assay can be “clinically validated” until the analyte has been shown to be *reproducibly* associated with disease. The quotes you copied and pasted from miscellaneous documents are all about clinical tests for pathogens that had already been found to be associated with specific diseases, such as HIV/AIDS. You’re demanding that we assume the Lombardi et al. results are unquestionably correct, and then only use assays that mimic their results. That’s a faith-based approach, not a science-based one.

The deafening silence about the Levy paper is also rather telling. They re-tested the same samples, using some of the same assays as Lombardi et al. but controlling carefully for contamination, and found they were all XMRV-negative. Be sure you read all the way to the acknowledgements on that one, where they thank “D. Peterson” for providing the samples. That’s Peterson as in Whittemore-Peterson Institute. Are you going to claim he’s part of the conspiracy, too?

None of the negative papers have clinically validated any of their assays. The Lombardi consortium did. The negative papers have only optimised for analytical sensitivity. You pretend there are no clinical positives, but what you really mean is that you don’t want there to be any until it is a researchers you approve of confirms the finding. Well this obviously has its own problems and is totally wrong.

Take this article from the WHO into this very issue about how to get clinical positives. The Lombardi team did this.

“Non-commercial or ‘in-house’ reference standards are legitimate only if they have been adequately validated. Sometimes, composite reference standards might have to be used in the absence of a single suitable reference standard. Results from two or more assays can be combined to produce a composite reference standard6.”

“External validation can be performed by sending all positive specimens and a proportion of the negative specimens to another laboratory for testing.”

http://www.nature.com/nrmicro/journal/v8/n12_supp/full/nrmicro1523.html

And there is this from the FDA:

“Clinical validation of these preliminary assessments is then accomplished through field testing of appropriate clinical specimens to provide final specifications for test kit performance characteristics.”

“A minimum of 10 distinct HIV positive specimens obtained from different individuals would be advisable for each subtype/variant. In the event that 10 distinct clinical specimens of a specific viral subtype are not available, culture derived specimens may be used to supplement clinical samples.”

“A minimum of 200 samples known to be positive for HIV-2 should also be tested in the evaluation of clinical sensitivity for single donation screening tests, including a subset that contain both HIV-1 and -2. These samples may be obtained from a repository.”

http://www.fda.gov/biologicsbloodvaccines/guidancecomplianceregulatoryinformation/guidances/blood/ucm077067.htm

The evidence is therefore pretty overwhelming that the original paper has not been challenged at all. No replication or validation.

The Coffin paper is also terribly flawed and full of enormous holes. It should never have been published anywhere. All they have done is squander time and money.

@Sam This nonsensical talking point about “validated assays” is really annoying. Repeating it every few weeks, as you and the other WPI acolytes do, doesn’t make the argument any more reasonable. The negative studies have done just as much validation as Lombardi et al. and Lo et al. on their assays. Demanding “clinically validated” assays is just silly, because the crux of the matter is whether there are in fact any real clinical cases of XMRV infection. The evidence is now pretty overwhelming that there are not. As for the Coffin paper, it’s open access, so folks can just go read it themselves to see how thorough it is. I suggest they also check out Levy’s paper, released at the same time, which drives another big stake through the heart of the XMRV-causes-anything theory.

The Coffin paper on origin is also absent a few crucial details, which without cannot prove the virus was created during xenografting. For instance, it is not clear if the mice that they find this claimed preXMRV1 & 2 in were even used. They have not checked wild mice for PreXMRV 1& 2. There are other ancestral viruses for XMRV in wild mice. Finally, their is no proof that their assays can detect the virus. So the earlier generations, not treated with testosterone, can still contain XMRV. Testosterone will increases the titre of the virus massively, so to a detectable level. But we know this is not what the virus does in a natural infection.

There is also no attempt to explain the other strains identified. The polytropic and modified polytropic. Both of which Lo et al and the WPI have sequences for in the GenBank.

So no the virus is human and replicating and still associated with prostate cancer and ME.