It's an interesting question that I've been thinking about since Dr Martin Lerner recently reported successfully treating people with CFS with anti-virals. Lerner was testing for, and treating, the Herpes family of viruses (EBV, HCMV, HHV-6) with valacyclovir (Valtrex) or valgancyclovir (Valcyte).
It seems to me that the possibilities are as follows:
1. XMRV could work in a similar way to HIV. When an HIV patient's illness progresses, the symptoms that are experienced are due to the opportunistic nature of our everyday viruses, such as HHV-6. Indeed, if my memory serves me right, one of the herpes viruses was first discovered due to infection in HIV/AIDS patients. In the case of Martin Lerner's studies, it could be that his anti-virals are successfully treating the secondary, opportunistic, viruses such as HHV-6 but that XMRV stays within the body. The opportunistic Herpes viruses might directly be causing the symptoms, rather than the XMRV. On it's own, without opportunistic secondary infection, XMRV infection might not cause any illness symptoms. After the Herpes viruses have been treated, the patients' natural bodily defenses may then be able to naturally keep the worst of the XMRV damage at bay (or to naturally keep the viral load low), due to a strengthened immune system, just as there are people who are XMRV carriers, but who are not ill with CFS, according to the Science paper.
2. It might be a lucky coincidence that the anti-virals that Martin Lerner is using actually kills the XMRV virus, or indirectly leads to a reduction in viral load, but no one has studied this effect of these anti-virals yet. The possible coincidental reduction of XMRV due to treatment with these anti-virals maybe the reason for the 'recovery' experienced by patients (i.e. a reduction of XMRV viral load leads to recovery). I don't know if anyone has yet tested valacyclovir (Valtrex) or valgancyclovir (Valcyte) directly on XMRV, but even if these drugs are thought to be ineffective at directly killing XMRV, they might still indirectly lead to a reduction of the viral load of XMRV through processes not yet known about. (I'm not up-to-date on all the research, and there's so much info to retain, that I can't hope to remember it all anyway!)
3. It maybe that CFS/ME is not caused by either XMRV or Herpes virus infections, but that these are both opportunistic infections which take hold in a weakened immune system caused by some not yet understood disease process. Treating the Herpes viruses with anti-virals may allow a patient's body to strengthen its natural defenses, and to possibly 'reset' the body's defense system, and maybe this is what leads to a recovery. (XMRV may yet be proved to be a passenger virus in a previously weakened immune system.)
4. Or another possibility (and i've added this since reading the next post - Hope's post) is that those patients treated with anti-virals for Herpes family viruses, by Dr Lerner, might not have had any XMRV infection, but that particular ME/CFS cohort could have some other cause, such as a prolonged HHV-6 infection or some other immune system disruption.