The role of antibody in recovery from experimental rabies. I. Effect of depletion of B and T cells.
The avirulent high egg passage (HEP) strain of rabies virus produces an inapparent infection limited to the central nervous system (CNS) in intracerebrally inoculated adult mice. Heavy 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 cell function is normal when measured by the concanavalin A response of splenic lymphocytes. This indicates that the B 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, the data suggest that cellular immune mechanisms may also contribute to host defenses against this central nervous system (CNS) virus infection.
D000818:Animals; D000917:Antibody Formation; D000961:Antilymphocyte Serum; D001402:B-Lymphocytes / Q000276:immunology*; D001921:Brain / Q000382:microbiology; D003520:Cyclophosphamide / Q000494:pharmacology; D007111:Immunity, Cellular; D008212:Lymphocyte Depletion; D051379:Mice; D011818:Rabies / Q000276:immunology*; D011820:Rabies virus / Q000528:radiation effects; D013601:T-Lymphocytes / Q000276:immunology*; D013950:Thymus Gland / Q000601:surgery; D014779:Virus Replication; D014965:X-Rays
D000961:Antilymphocyte Serum; D003520:Cyclophosphamide