PROPHYLACTIC ACYCLOVIR EFFECTIVELY REDUCES HERPES-SIMPLEX VIRUS TYPE-1 REACTIVATION AFTER EXPOSURE OF LATENTLY INFECTED MICE TO ULTRAVIOLET-B

Purpose. To determine the potential efficacy and anatomic sites of act ion of prophylactic oral acyclovir using a murine model of ultraviolet -B-induced reactivation of herpes simplex 1 keratitis. Methods. Latent infection with herpes simplex 1 (McKrae) was established in 80 Nation al Institutes of Health inbred strain of mice. Forty of the mice were given acyclovir orally and the other 40 latently infected mice served as controls. Mice were exposed to 250 mJ/cm2 of ultraviolet-B radiatio n and killed on days 1, 2, 3, and 4 after ultraviolet-B radiation. Tri geminal ganglia and eyes from these mice were homogenized and incubate d on Vero cell monolayers for recovery of reactivated virus. Results. Based on the recovery of infectious virus after ultraviolet-B in treat ed versus control groups, acyclovir effectively reduced detectable vir al reactivation at both the ocular level (P = 0.003) and the ganglioni c level (P = 0.025). The numbers of viral culture-positive eye and tri geminal ganglia homogenates in the control group were 11 and 6 out of 40, respectively, compared to 1 and 0 out of 40 culture-positive eye a nd trigeminal ganglia homogenates in the acyclovir treated mice. Thera peutic serum levels of acyclovir were confirmed by high performance li quid chromatography. In the acyclovir-tested group, the single case of viral breakthrough at the ocular surface was not an acyclovir-resista nt mutant. Conclusion. Prophylactic acyclovir effectively reduces the incidence of herpes simplex virus-I reactivation after ultraviolet-B-i nduced reactivation in National Institutes of Health inbred strain of mice.