However, when we administered BALB/c mice a low dose to simulate latent infection in humans, the DNA copy number, pathological damage and viral reactivation ability of the mutant strain were lower than those of the LAT-HSV-2 and wild-type virus strains, which also means that the HSV-2 mutant strain lacking both RL1 and LAT genes has a diminished ability to establish latency. The gene discussed is LAT; the disease is disease arising from reactivation of latent virus.