Abstract
Abstract
A series of investigations was designed to study the role of cellular immunity, humoral antibody, and interferon in recovery from primary systemic herpes simplex virus type I (HVH) infection in mice. Nude and neonatally thymectomized mice, which have a specific defect in T-cell function, were dramatically more susceptible to primary systemic HVH infection. These immunosuppressed mice did not form neutralizing antibody to HVH, and had pathological lesions involving primarily the liver and brain. Passive transfer of physiologic amounts of neutralizing antibody after infection largely protected these T-cell-deficient HVH-infected mice. The results thus suggest that the formation of anti-HVH antibody in the nonimmunosuppressed mouse is critically important in promoting recovery from systemic HVH infection. The findings do not favor a dominant defensive role for immune cells, but they do not exclude a defensive role for these cells in this experimental primary HVH infection.
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