As we currently lack postulates to prove a causal association with a prevalent agent and a chronic disease with genetic predisposition, it would also be appropriate to conduct interventional studies. Indeed, the Helicobacter pylori hypothesis of peptic ulcer disease was only accepted after Barry Marshall showed that bacterial eradication with antibiotics cured peptic ulcer disease (21). Studies to gain proof of principle have been performed with antivirals in other chronic, idiopathic diseases linked to retroviral infection, such as primary biliary cirrhosis associated with mouse mammary tumor virus, another possible murine zoonosis (22). Trials using a combination of reverse transcriptase inhibitors led to significant improvements in clinical, histological, and biochemical outcomes in these patients, albeit with some evidence of viral resistance to therapy (23). Such studies are now feasible for CFS, because reverse-transcriptase inhibitors, such as tenofovir and emtracitabine, and the integrase inhibitor raltegravir can inhibit XMRV (24).
Indeed the multiple origins of these xenotropic sequences, the hybrid nature of the XMRV genome, and the occlusion of the otherwise necessary glycogag ORF underscore the potential complementation and recombinational events that may lead to their transmission into humans. ... These observations suggest a scenario in which retroviruses, MLV-related agents, and potentially, other viral agents may cross-complement to promote coinfection and enable pathogenicity.
By mentioning MMTV they indirectly bring in a possible HMTV, without explicitly mentioning relevance to breast cancer research. The implications keep growing....such as primary biliary cirrhosis associated with mouse mammary tumor virus, another possible murine zoonosis...