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• W2314414323 abstract "Treatment with rabbit or horse antiserum to murine thymocytes (antithymocyte serum or ATS) potentiated primary systemic infection with vaccinia virus in mice. Formation of serum neutralizing antibody was suppressed and viremia was prolonged by treatment with ATS. This potentiation of vaccinia virus infection by ATS treatment was largely reversed by passive transfer of physiologic amounts of antibody late in the course of infection, at a time when nonimmunosuppressed mice had neutralizing antibody in their sera. The concentration of interferon in serum was not affected by treatment with ATS. These results suggest a critical role for antibody, but not for cellular immunity, in recovery of mice from primary systemic infection with vaccinia virus. The relative importance of cellular immunity, humoral antibody, and of nonimmune factors, such as interferon, in recovery from a primary viral infection has not been established. In recent years evidence from both infections in man and experimental studies has been interpreted to suggest a crucial role for cellular immunity and a less important role for humoral antibody in this recovery process, particularly for vaccinia virus infections [1-3]. To test this hypothesis, I have conducted a series of studies to determine the effect of a number of different immunosuppressive agents on primary vaccinia virus infection in mice. These studies have suggested that humoral antibody, but not cellular immunity, is critical in recovery from primary vaccinia virus infection in mice [4]. The present communication specifies the effect of horse and rabbit antisera to murine thymocytes (antithymocyte serum or ATS) on the course of primary vaccinia virus infection of the mouse." @default.
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• W2314414323 date "1973-05-01" @default.
• W2314414323 modified "2023-09-24" @default.
• W2314414323 title "Mechanism of Recovery from Systemic Infection with Vaccinia Virus. III. Effects of Antithymocyte Serum" @default.
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• W2314414323 doi "https://doi.org/10.1093/infdis/127.5.518" @default.
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