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3 different types of observation all demonstrated that B virus (Herpesvirus simiae) infection of monkeys was not confined to the mouth but was also a genital infection. (1) Latent B virus was reactivated in a seropositive female monkey, which was immunosuppressed with antilymphocyte globulin, and infectious virus was excreted in the genital tract. (2) During an epizootic in a breeding colony, B virus was isolated from 4 genital and 3 oral sites as well as from a skin lesion. (3) In cultures of sensory nerve ganglia taken from seropositive monkeys, B virus was recovered more frequently from ganglia subserving the genital region than the oral region.

Studies of B virus (Herpesvirus simiae) antibody in several species of macaque lead to the following generalizations. Newborn monkeys are not infected with B virus, even when born of seropositive mothers. Young monkeys remain uninfected until they become adults. The majority of adults develop B virus antibody unless their physical contact with seropositive adults is restricted. These observations are consistent with sexual transmission of B virus and classification of the disease in monkeys as venereal. However, infection at oral and dermal sites also occurs and may play a part in monkey-to-monkey transmission. Epizootics of B virus occurred during early attempts to start B virus-free breeding colonies. They appeared to originate from reactivated latent B virus in adult monkeys which had only low titres of antibody. The stress produced when groups of adult strangers were assembled to form breeding colonies was the most effective known inducer of latent B virus. Total exclusion of animals with any trace of antibody has enabled the establishment of new breeding colonies which are free from B virus.

Local infiltration of antiserum into sites inoculated with B virus protected rabbits from an otherwise fatal encephalomyelitis. Treatment was effective when delayed for six hours but not after 24 hours. Homologous rabbit antisera were more effective than heterologous monkey antisera, and protection was unrelated to neutralisation titres. Protection apparently depended not on neutralisation of inoculated virus but on destruction of infected cells before they produced progeny virus. Normal human immunoglobulin able to neutralise B virus did not protect. Intravenously administered antibody was effective only if large doses were given. The findings suggest that persons bitten or scratched by monkeys latently infected with B virus may be treated successfully by immunoprophylaxis with specific antibody. Stocks of human or of more readily available simian antisera should be held in laboratories where such animals are used.