Expression of immunity to intravaginal herpes simplex virus type 2 infection in the genital tract and associated lymph nodes.
Herpes simplex virus type 2 is a human venereal pathogen which causes lethal neurological illness after intravaginal inoculation into BALB/cJ mice. In the present studies, we demonstrate that intravaginal vaccination with an attenuated strain of this virus, which possesses a partial deletion of the thymidine kinase gene, rapidly induced durable immunity to lethal intravaginal challenge with wild-type virus. Such immunity was characterized by a dramatic hyperplasia of genital lymph nodes and a significant reduction in wild-type virus replication and spread from the genital tract following lethal challenge. Of greater importance, immunity to lethal wild-type virus challenge in the genital tract was transferrable to non-immune mice with genital lymph node cells prepared 1 week after intravaginal vaccination but was not transferrable with serum or cells from other lymphoid organs tested at this time. The adoptive transfer of anti-viral immunity to wild-type challenge was also characterized by a diminution in wild-type virus replication and spread from the genital tract. These results suggest that an important component of cellular immunity to genital pathogens may be antigenic stimulation of genital lymph nodes.
D000367:Age Factors; D000818:Animals; D001921:Brain / Q000382:microbiology; D005260:Female; D005727:Ganglia, Spinal / Q000382:microbiology; D006558:Herpes Genitalis / Q000276:immunology* / Q000382:microbiology / Q000473:pathology; D007111:Immunity, Cellular; D007114:Immunization; D007116:Immunization, Passive; D008198:Lymph Nodes / Q000276:immunology / Q000473:pathology; D008213:Lymphocyte Activation; D051379:Mice; D008807:Mice, Inbred BALB C; D013116:Spinal Cord / Q000382:microbiology; D014627:Vaginitis / Q000276:immunology / Q000382:microbiology