DEFENSE-MECHANISMS AGAINST PRIMARY INFLUENZA-VIRUS INFECTION IN MICE .1. ROLES OF INTERFERON AND NEUTRALIZING ANTIBODIES AND THYMUS DEPENDENCE OF INTERFERON AND ANTIBODY-PRODUCTION

  • 1 January 1977
    • journal article
    • research article
    • Vol. 118  (1) , 256-263
Abstract
To investigate the defensive roles and production of interferon and antibodies, C3H/He mice were subjected to various immunosuppressive treatments and infected with influenza virus. In infected normal control mice the pattern of pulmonary viral growth can be divided into 3 phases. The 1st phase is characterized by an exponential increase of virus titer, the 2nd by a rapid decrease and the 3rd by a moderate decrease. At the time of transition from the 1st phase to the 2nd in pulmonary virus growth, interferon could be detected in the tracheobronchial washings of infected mice, but neutralizing antibodies could not. In infected B [bone marrow-derived] cell-deprived mice and infected anti-.mu.-treated mice, the transition from the 1st phase to the 2nd occurred without any detectable antibody production, and interferon could be induced in the early stage of infection. The pulmonary virus in these mice increased again exponentially until the death of the mice. In infected T [thymus-derived] cell-deprived mice which could not induce interferon, but produced Ig[immunoglobulin]M-neutralizing antibodies, the 2nd phase was not observed after the 1st phase, but a transient plateau phase could be demonstrated, and then the pulmonary virus increased again exponentially until the death of the mice. In anti-.gamma.-treated mice, pulmonary virus growth and production of interferon and neutralizing antibody were almost similar to those of infected normal control mice except for the absence of IgG neutralizing antibody production. Although anti-.alpha.-treated infected mice produced interferon and no IgA antibody, the transition from the 1st exponential increase of pulmonary virus to the 2nd rapid decrease was seen, but the virus increased exponentially again until the death of the mice. Interferon apparently plays an important role in the transition from the 1st phase to the 2nd. T cells are apparently required for interferon induction in mice infected with influenza virus. IgA antibodies probably play an important role in the inhibition of virus propagation in the lungs after the disappearance of interferon. Infected T cell-deprived mice could produce only IgM neutralizing antibodies, but not IgG and IgA antibodies. T cells are required for the production of IgG and IgA antibodies and eventually for defense functions in mice infected primarily with influenza virus.