Ability of herpes simplex virus (HSV) types 1 and 2 to induce clinical disease and establish latency following previous genital infection with the heterologous HSV type.

Guinea pigs were infected intravaginally with either herpes simplex virus type 1 (HSV-1) or type 2 (HSV-2). One month postinoculation, animals were inoculated with the heterologous HSV type and observed for clinical disease and shedding of virus. One month after superinfection, animals were killed, and tissues were cocultivated to detect latent virus. Although the severity of clinical disease and the degree of shedding of virus were greatly reduced by prior infection with the heterologous virus type, superinfection did occur in 82%-90% of animals. Nervous system latency with the superinfecting virus was established in 20% of animals superinfected with HSV-2 and 55% superinfected with HSV-1. Of 21 animals tested, 5 had latent infection with both viruses, 6 with the superinfecting virus only, and 6 with the initial virus only. Protection from nervous system latency with the superinfecting virus correlated best with levels of serum neutralizing HSV antibody before superinfection.