ROLE OF ANTIBODY IN RECOVERY FROM EXPERIMENTAL RABIES .1. EFFECT OF DEPLETION OF B-CELL AND T-CELL

Abstract

The avirulent high egg passage (HEP) strain of rabies virus produces an inapparent infection limited to the CNS in intracerebrally inoculated adult mice. H chain isotype (anti-.mu. antiserum) immunosuppression potentiates the infection, with a mortality of about 60% and with elevated virus titers in the brain. Anti-.mu.-treated mice fail to raise antibody responses to rabies virus although their T [thymus derived] cell function is normal when measured by the concanavalin A response of splenic lymphocytes. This indicates that the B [bone marrow derived] cell response plays an important role in clearance of rabies virus from the neuroparenchyma. Treatment with cyclophosphamide or by adult thymectomy, X-irradiation and bone marrow reconstitution potentiates HEP infection to a greater extent than does isotype suppression. Since these suppressive techniques impair both T and B lymphocyte responses, cellular immune mechanisms may also contribute to host defenses against this CNS virus infection.