Not sure if anyone has gone down this track. If XMRV is propagated via immune system activation, possibly due to secondary virus or viral load, then could this be the major difference between sudden and gradual onset XMRV. If the Lake Tahoe cohort was also infected with a rapid onset virus which ignited XMRV replication, then what will be significant is not just that they had XMRV but what that secondary trigger virus was. Genetics as a determinant does not explain why everyone in the Tahoe group came down with rapid onset (unless they were all cousins, of course). Far more likely that the group already had XMRV which is slow to replicate under most circumstances, but the circumstance changed to induce rapid replication. And if not a secondary virus, perhaps some other trigger. Perhaps when the dust is settled on the XMRV issue someone will look closely at the triggers. Maybe categorise them according to how effectively they contribute to XMRV propagation. For example EBV may be a slow trigger or CMV a rapid trigger and so forth. Or a measles vaccination may be a rapid trigger.