The key argument for XMRV being a contaminant has nothing to do with how XMRV was created or where it came from. These people aren't idiots...they know that dangerous viruses can and have been produced in labs before
http://news.bbc.co.uk/2/hi/health/3719990.stm
But that link is not at all relevant to the significance of the way that XMRV was created.
The link you give describes a
deliberate and controlled experiment in which a flu virus was genetically modified in such a way as to make it deadly. The argument about how XMRV was created says that it turns out that a human retrovirus was
accidentally created during a standard laboratory process, and that this retrovirus has spread worldwide through cell cultures, in such a way that many laboratories are contaminated with it...and the precise routes of such contamination remain mysterious.
Scientists may, perhaps, have all been well aware that standard laboratory work has been creating novel human retroviruses, spreading them around the world, and contaminating laboratory experiments (at least) through unknown vectors, but it was news to me and I think many people would be very interested to learn that this is the case - especially those still curious about the origins of the HIV virus.
As a general proof of concept, it's
surely significant that such previously undetected retroviruses have been created and spread through laboratories in this way...especially to someone who is wondering what might be the cause of unrecognised new forms of neuro-immune disease, and especially to someone who is wondering whether a contaminated vaccine may have been what made them or their child sick.
But I'll repeat that the implications of the idea that any such retroviruses may have been responsible for human disease, and/or may have been transmitted in vaccines, are so dramatic and unthinkable that they are hard possibilities for scientists to face up to - even though such possibilities are perfectly plausible and demand further investigation.
The key factor is that the XMRV found in the WPI samples is so genetically similar to that found in the 22RV1 lab strain that it simply could not have made it into the human body. If it had made it into the human body it would have shown signs that that had happened.
This genetic similarity is presumably in reference to the 2.5 XMRV samples that the WPI sequenced fully, and now (but not when the argument was originally advanced as definitive) in reference to the sequences subsequently submitted by the WPI, which do show
some variability.
The argument requires several assumptions, of course: that those 2.5 samples are representative of all the XMRV detected by the WPI; that the specific tests employed by the WPI are not just picking up a well-defined subset of the strains present; and crucially, that if XMRV had made it into the human body it would have reproduced and mutated just as expected, and does not exhibit properties of sequence conservation. There may be a cast-iron argument proving the latter assumption, but I haven't seen it yet, and we do need to see that argument. What I
have seen is a convincing assertion that slow-replicating retroviruses, viruses exhibiting sequence conservation properties (as proven for XMRV under APOBEC3 editing), and viruses with short genetic sequences, can be expected to show much lower levels of mutation than other viruses. And it's always made sense to me that a virus defined by such a short genetic sequence is likely to show relatively low levels of variability.
So while this argument does seem strong, it also seems to be statistical, and based on assumptions, and does not seem at all conclusive to me. Ranged against arguments like the absence of any known vector for contamination of WPI samples, the absence of any evidence of XMRV contamination of any product used by the WPI or other labs that found XMRV, and of course the consistent differential rates of detection between patients and controls, it still leaves a lot of questions to be answered.
If the XMRV samples from the WPI and from prostate cancer samples were more genetically distinct it wouldn't matter where they came from. The fact that researchers can show XMRV was probably produced in a lab in the 90's simply explains things...it helps to tie things together.
Of course there's a Catch-22 here: the strains of pMLVs sequenced by Lo and Alter
are genetically distinct from XMRV - though less distinct than different strains of HIV-1 - and were therefore said to be nothing to do with XMRV. Heads I win, tails you lose?...
The NCI just posted a statement on their website that they have isolated strains of XMRV from the original samples and those strains, contrary to the WPI's assertion, indicate that XMRV has never entered the human body.
I read that but I didn't see the reasoning behind this assertion. Is that also based on them finding that all the strains they isolated had the same low levels of genetic diversity, or on some other evidence? And did they detect the same kind of variants that the WPI have shown in the sequences recently submitted to GenBank? Those details seem to be crucial to this argument, so I guess we'll need to see those in order to be convinced...
While I'm on...am I right in saying that the entire question of "mouse contamination" is a complete red herring, and that all those tests for mouse contamination, IAP tests etc, were barking up the wrong tree? Because the contamination that is alleged is from
cell lines in laboratories, which are themselves systematically infected with XMRV, and it has nothing to do with mice at all except that XMRV itself was originally created inside a mouse. In which case, I don't understand why Dr Coffin was recently speculating about mice roaming around and carrying lab material from lab to lab on their fur, because his own argument makes that vector for contamination seem quite irrelevant now. And the suggestions that the WPI's labs themselves are contaminated also seem irrelevant, along with all the tests for mouse DNA, because there's no reason at all to suggest that such contamination would be a factor if the XMRV is all supposed to come from cell lines.
It's been said before and it will be said many times again I'm sure: this will not be over until all the details are fully explored, explained, and accepted by the WPI. Having got so far, the job of explanation should - must - be completed: leaving crucial questions hanging will only fuel a thousand conspiracy theories for decades to come. So the next job for the contamination theorists must surely be to identify the source of contamination in the WPI's process, and to explain the contamination's preference for samples from people with ME/CFS? Given that others have detected XMRV in WPI samples, in multiple labs (including Blomberg's notable detection of XMRV in a WPI sample), it remains the case that the only plausible source of contamination was during the blood collection process, most likely via contamination of the specific type of collection tubes used by the WPI. So XMRV now has to be sought in those tubes: if they contain XMRV to start with then this needs to be understood.
And critically, what remains to be explained is how the WPI are consistently finding differences in XMRV detection between different groups. Supposing that the tubes they used are all contaminated with XMRV, it would still be possible that some property of ME/CFS patients' blood is responsible for the different levels of detection of XMRV by the WPI. That would be vital to understand and could be a breakthrough in itself. So the absolute bottom line for me remains: the WPI remain solidly convinced that they are detecting different results from ME/CFS patients as opposed to healthy controls, and there is still no reason whatsoever to imagine this is due to incompetence on their part, and so this difference in detection rates demands a full explanation - after everything we've all been through with this, it would be completely crazy to just stop now and walk away from all those unanswered questions.