Immunosuppression promotes ocular virus replication and CNS neurovirulence following corneal inoculation with an avirulent herpes simplex type 1 thymidine kinase negative mutant

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Abstract
The effect of immunosuppression on the pathogenicity of an avirulent HSV-1 [herpes virus type I] thymidine kinase negative mutant was studied in the murine model. Following corneal inoculation with an HSV-1 TK- mutant, normal and cyclophosphamide-immunosuppressed outbred mice were evaluated for keratitis, ocular, trigeminal ganglia, and forebrain virus titers, survival, and latency. Immunosuppression enhanced virus pathogenicity producing greater keratitis, higher ocular, trigeminal, and forebrain virus titers, decreased survival, and increased trigeminal ganglionic residual infectious virus and latency. Apparently, normal host defenses as well as the virus thymidine kinase expression contribute to HSV-1 pathogenicity.