A sentence from the paper caught my eye, "Furthermore, we have affirmed that the likely receptor, xenotropic and polytropic retrovirus receptor 1 (XPR1), is required for XMRV infection, and we have determined the first integration sites of XMRV in human genomic DNA isolated from tumor-bearing prostatic tissue, thus validating that humans have been infected with this virus."
You could develop a drug to bind preferentially to this receptor or one to duwnregulate it's activity but only if it's redundant (it's task can be filled by other similar receptors) or fairly unimportant to physiology. I don't know enough myself to say more than that. Perhaps better is to find something the virus itself would bind to instead, the way e. Coli bacteria in the bladder bind to the mannose in cranberry instead of the mucosal lining.
To my mind its to early to say whether XMRV - assuming it is proven to be the primary causal mechanism behind the varying presentations of CFS - uses cell infection as its primary pathological mechanism. Retroviruses could also result in chronic inflammation, could cause epigenetic changes to the DNA that governs immuno and autonomic control (HIV has been found to make a number of epigenetic changes to the DNA of sufferers), and a whole host of other possibilities.