LAT and disease arising from reactivation of latent virus: The virus loads of LAT mutant strains in the brain and spinal cord tissues post latent infection even exceeds that of wild strains, this may be due to the strict suppression of virus lytic gene replication as the LAT gene is present [36,37], but when the LAT gene is deleted alone, the latent state may be broken, resulting in a small amount of lytic gene replication occurred in the virus, which increased the viral loads of LAT-HSV-2 infected mouse tissues.