Taken together, these data indicate that B cell-intrinsic IL-17RA signaling not only promotes the MHV68-driven germinal center response (Fig. 3), but it also supports MHV68 latent infection of germinal center B cells as the attenuation of the germinal center response alone (~2-fold decrease) in MHV68-infected CD19 Cre-positive does not fully account for the over eightfold decrease in MHV68 latently infected cells in the spleen. The gene discussed is IL17RA; the disease is disease arising from reactivation of latent virus.