Not sure how you get from the first statement to the second statement. Most of what you are saying is very vague and is noteable by many omissions. If we are to educate specialists, then I suggest a few pertinant facts should not be omitted. If we exclude the VP62 plasmid, then there is no evidence whatsoever that a well designed PCR could not find HGRVs. If the negative studies focussed on VP62, then they should be negated themselves. In the BWG it appears that the WPI and VIPdx did not used their regular assays, supposedly because of the constraints of the BWG. So their assays have not really been challenged. The WPI lab assays in particular have not been challenged. Furthermore by only mentioning PCR, you neglect to mention that other methods, eg culture and serology, have not been challenged. Again WPI and VIPdx by necessity culture the virus, as they acknowledge it is difficult to find in the blood. All you are really saying is that so far the negative studies and the BWG have supported what WPI has been saying all along: the virus is hard to find in the blood and you need good assays. There is no proof yet that the virus is transmitted by blood; there are plenty of other vectors: placental transmission, vaccination, tissue transplantation, semen etc have not been ruled out. As for blood transmission, there is evidence that indicates that HGRVs are present in the blood during amplification stages only, and retreat to tissue reservoirs, during non-amplification periods, so they may only be transmissable by blood during the amplification period. Finallly, very strong models for a single retrovirus to cause different pathologies already exist. There is also new evidence that newly identified HIV strains, as yet unidentified by PCR, can have unique pathologies, thus providing an explanation for different subsets of ME. This behavior is also well characterised in MLV studies. In fact what the latest HIV study has found is that multiple pathologies, caused by multiple strains, can co-exist in a patient.