Roles of different T-cell subsets in control of herpes simplex virus infection determined by using T-cell-deficient mouse-models.
Herpes simplex virus infection of the scarified dermis results in infection of the nervous system and, subsequently, a cutaneous lesion in the innervated dermatome. We compared the pathogenesis of such zosteriform lesions in mice lacking or severely depleted of CD4+ or CD8+ T cells because of targeted gene disruption. Mice without CD4+ cells showed markedly increased susceptibility, whereas beta 2 microglobulin knockout mice lacking CD8+ T cells were as resistant to challenge as were immunocompetent mice with the same genetic background. Our results demonstrate that CD4+ T cells are of primary importance in the control of herpes simplex virus infections of the skin and nervous system.
D000818:Animals; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology; D004198:Disease Susceptibility; D006558:Herpes Genitalis / Q000276:immunology*; D006561:Herpes Simplex / Q000276:immunology*; D018259:Herpesvirus 1, Human / Q000472:pathogenicity; D018258:Herpesvirus 2, Human / Q000472:pathogenicity; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D013045:Species Specificity; D016176:T-Lymphocyte Subsets / Q000276:immunology*; D001613:beta 2-Microglobulin / Q000172:deficiency / Q000276:immunology
D001613:beta 2-Microglobulin