We showed that during latent infection, KSHV elevated Beclin phosphorylation and enhanced autophagic flux as measured by an increase in LC3 puncta size and the accumulation of the lipidated form of LC3-II after Bafilomycin treatment and that LC3-II accumulation during KSHV latency required KapB and MK2. This evidence concerns the gene MAP1LC3A and disease arising from reactivation of latent virus.