THE HOST RESPONSE TO HERPES SIMPLEX VIRUS

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Abstract
The article reviews experimental herpes; much of the work has been done in the laboratory mouse. The acute primary infection and translocation of virus to the local sensory ganglion is more complex than previously supposed. The nature of latency, persistence, reactivation, recurrence and recrudescence are discussed. At least three immunological responses contribute to the clearance of virus: antibody, specific cytotoxic T cells and specific delayed hypersensitivity. Antibody hinders the establishment of persisting infection and, in high concentration, may pervent invasion of the nervous system. T cells are essential for protective immunity but which type is more important is unclear. The nature of ganglionic latency is still enigmatic and what controls the state is unknown. There is no clear evidence that immunological mechanisms are involved. The fate of reactivated virus and the development of recrudescent lesions seems to be under immunological control and has been studied to good effect in the guines pig. There is insufficient direct information about the immunological control of herpes in man and any conclusions including decisions on the use of vaccines in man still depend in large measure on animal experiments.

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