Reduced latent infection of MLNs by mLANA-null virus, but only minimal impact on O73.loxP infection of CD19Cre/+ mice, suggests the possibility that mLANA functions in non-B cells to permit efficient trafficking to the lung, or is necessary for seeding and expansion of B cells in the MLN after trafficking. This evidence concerns the gene MLANA and disease arising from reactivation of latent virus.