Respiratory syncytial virus infection in anti-mu-treated mice.
BALB/c mice were depleted of B cells by anti-mu treatment to investigate the pathogenesis of respiratory syncytial virus (RSV) infection in the absence of antibody. Termination of RSV replication after primary infection occurred with the same kinetics in anti-mu-treated mice as in phosphate-buffered saline (PBS)-treated controls. Yet, when rechallenged, anti-mu-treated mice were more permissive to RSV replication than PBS-treated controls. Anti-mu-treated mice also experienced greater illness than PBS-treated controls during both primary infection and rechallenge. Passive transfer of RSV-specific immune serum to anti-mu-treated mice before rechallenge reconstituted complete protection from RSV replication and diminished illness. Thus, RSV-specific antibody is not required to terminate RSV replication in primary infection, but without antibody, only partial immunity against rechallenge is induced. While it is unknown whether the mechanism is a direct effect on RSV titer or modulation of the illness-causing cellular immune response, the presence of RSV-specific antibody reduces illness in both primary RSV infection and rechallenge of mice.
Graham
B S
BS
Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee 37232-2605.
Bunton
L A
LA
Rowland
J
J
Wright
P F
PF
Karzon
D T
DT
D000818:Animals; D000888:Antibodies, Anti-Idiotypic / Q000276:immunology; D000914:Antibodies, Viral / Q000276:immunology; D000917:Antibody Formation; D001402:B-Lymphocytes / Q000276:immunology*; D007148:Immunoglobulin mu-Chains / Q000276:immunology; D007156:Immunologic Memory; D008168:Lung / Q000473:pathology; D051379:Mice; D008807:Mice, Inbred BALB C; D012136:Respiratory Syncytial Viruses / Q000254:growth & development* / Q000276:immunology; D010253:Respirovirus Infections / Q000276:immunology* / Q000473:pathology
D000888:Antibodies, Anti-Idiotypic; D000914:Antibodies, Viral; D007148:Immunoglobulin mu-Chains