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Rat monoclonal antibodies were used to deplete selectively Lyt 2 (cytotoxic) and L3T4 (helper) T cell populations in vivo. These antibodies produced greater than 95% depletion of the respective T cell subset as determined by fluorescent antibody and cytofluorographic analyses. Antibody-treated mice were infected in the ear pinna with herpes simplex virus (HSV) and the induction of virus-specific T cell and antibody responses were monitored during the acute infection. Lyt 2-deficient mice produced delayed hypersensitivity and HSV-specific antibodies comparable to those in untreated animals. However, major histocompatibility complex class I-restricted T cell killing was abolished. In contrast, L3T4-deficient animals failed to produce either primary delayed hypersensitivity response or specific antibodies to the virus, but cytotoxic T cell responses were induced and even augmented in comparison with infected, normal animals. This observation clearly demonstrates that Lyt 2 cytotoxic T cells can be induced in a helper T cell-deficient environment. The ability of T cell subset-deficient mice to clear infectious virus was investigated in the skin of the ear and the part of the nervous system innervating the site of infection. L3T4-deficient animals showed a markedly delayed clearance of virus from the ear and also had a more florid infection of the nervous system. However, Lyt 2-deficient mice cleared the infection in the ear normally, but a severe infection of the nervous system was still observed. The implication of these observations to the pathogenesis of this virus is discussed.

Original publication




Journal article


J Gen Virol

Publication Date



68 ( Pt 3)


825 - 833


Animals, Antibodies, Monoclonal, Antibody Formation, Cytotoxicity, Immunologic, Female, Herpes Simplex, Hypersensitivity, Delayed, Mice, Mice, Inbred CBA, Nervous System Diseases, Skin Diseases, T-Lymphocytes, T-Lymphocytes, Cytotoxic, T-Lymphocytes, Helper-Inducer, Thymectomy