The senescence-accelerated mouse shows aging-related defects in cellular but not humoral immunity against influenza virus infection.

Abstract

The senescence-accelerated mouse (SAM) strain P1, which has a short life span, was adopted as a murine model for an investigation of the pathogenesis of viral infection in elderly adults. After intranasal inoculation with influenza A virus, the SAM-P1 mice showed a higher rate of mortality, with prolonged virus growth in the lungs. The increased susceptibility was associated with impaired activity of both NK cells and virus-specific cytotoxic T lymphocytes. The production of interferon-gamma and interleukin-12 was significantly restrained, which suggests a partial deficiency of the T helper (Th) 1 cells. In contrast, the immunologic activity of the Th2 cells appeared to be functionally normal, judging from the release of large amounts of interleukin-4 followed by production of appropriate amounts of influenza virus-specific antibody. It is suggested that the elicitation of cellular immunity is an important and effective procedure for protecting the elderly from influenza virus infection.