• 1 January 1981
    • journal article
    • research article
    • Vol. 43  (1) , 153-159
Abstract
Unresponsiveness to delayed type hypersensitivity was induced in mice following an i.v. injection of herpes simplex virus. The principal tolerogens used were thymidine kinase-deficient virus mutants which grow poorly in vivo; UV-inactivated, and to a lesser extent, formalin-inactivated virus were also tolerogenic. The tolerance induced was specific for the virus type. Despite the tolerance to delayed hypersensitivity, anti-viral immunity is present as determined by rapid infectious virus inactivation. The mechanism of tolerance to herpes virus and the importance of these observations for viral disease pathogenesis is discussed.

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