During latency, there were increased numbers and proportions of infected LPMs in HP/MHV68 coinfected mice, which were also dependent on vitamin A. In contrast to acute infection, we found the IL-4 -mediated expansion of LPMs during acute infection was not sufficient to cause increased latent infection, perhaps because LPM numbers returned to homeostatic levels by day 28 after IL-4 treatment. This evidence concerns the gene IL4 and disease arising from reactivation of latent virus.