The role of cellular immunity, humoral antibody, and interferon in recovery from primary systemic infection in mice due to herpes simplex virus type 1 (HSV-1) was studied. Immunosuppression by three methods--each of which was sufficient to suppress humoral and cellular immunity--markedly potentiated primary systemic HSV-1 infection. Immunosuppressed mice did not form neutralizing antibody to HSV-1, but passive transfer of physiologic amounts of neutralizing antibody as late as day 6 after infection exerted a protective effect. Passive transfer of 10(8) immune spleen cells on day 3 after infection was only partially protective and did not thereafter reverse the effect of X-irradiation on HSV-1 infection. Furthermore, mice that received immune cells appeared to make sufficient antibody to explain the protective effect of the transferred cells. These results suggest that antibody to HSV-1 has a critical role in promoting recovery from primary infection in this model. The findings neither favor nor exclude a defensive role for immune cells in this experimental primary HSV-1 infection.

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