Graham B S, Bunton L A, Rowland J, Wright P F, Karzon D T
Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee 37232-2605.
J Virol. 1991 Sep;65(9):4936-42. doi: 10.1128/JVI.65.9.4936-4942.1991.
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.
通过抗μ治疗使BALB/c小鼠的B细胞耗竭，以研究在无抗体情况下呼吸道合胞病毒（RSV）感染的发病机制。初次感染后RSV复制的终止在抗μ治疗的小鼠中与在磷酸盐缓冲盐水（PBS）处理的对照中具有相同的动力学。然而，再次攻击时，抗μ治疗的小鼠比PBS处理的对照对RSV复制更敏感。在初次感染和再次攻击期间，抗μ治疗的小鼠也比PBS处理的对照经历更严重的疾病。在再次攻击前将RSV特异性免疫血清被动转移至抗μ治疗的小鼠可重建对RSV复制的完全保护并减轻疾病。因此，在初次感染中终止RSV复制不需要RSV特异性抗体，但没有抗体时，仅诱导对再次攻击的部分免疫力。虽然尚不清楚该机制是对RSV滴度的直接影响还是对致病细胞免疫反应的调节，但RSV特异性抗体的存在可减轻小鼠初次RSV感染和再次攻击时的疾病。
