Valerie Courgnauda, Jean-Luc Battinia,
Marc Sitbona,1, and Andrew L. Masonb,1
aInstitut de Gén étique Moléculaire de Montpellier, Centre National de la Recherche Scientifique, Unité Mixte de Recherche 5535, Universite Montpellier 1 and 2, F-34293 Montpellier Cedex 5, France; and bDepartment of Medicine, University of Alberta, Edmonton, AB, Canada T6G 2E1
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
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.
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.
Such studies are now feasible for CFS, because reverse-transcriptase inhibitors, such as tenofovir and emtracitabine, and the integrase inhibitor raltegravir can inhibit XMRV.
The caveats for conducting clinical trials in patients with CFS and MLV infection are that the potential benefits of treatment should outweigh the risks; also, studies should be conducted as randomized
controlled trials with meaningful and feasible endpoints using robust therapies.
At this juncture, studies to establish proof of principle are justified to determine whether safe antiviral regimens can impact on CFS and to determine whether xenotropic or polytropic MLV is causally associated with this debilitating disease.
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