Abstract
Abstract Conventional influenza vaccines aim at the induction of virus-neutralizing antibodies. Influenza viruses can escape neutralization by antibodies through antigenic drift or shift or because antibody levels diminish. We wondered to what extent infection-permissive immunity provided by a trivalent inactivated influenza virus vaccine (TIV) could modulate disease and virus-induced host immune responses after homologous H1N1 infection. We first focused on alveolar macrophages, cells that are transiently lost during influenza infection in the mouse-influenza challenge model. Later we focused on how vaccine-induced immunity modulates induction of cross-reactive CD8+ T cells by virus infection. TIV vaccination did not result in detectable HI titers but correlated with lower viral lung titers and faster recovery after challlenge. Alveolar macrophages were abolished at 7dpi in negative control mice, but not in TIV-vaccinated mice. TIV vaccination allowed the induction but also affected levels of cross-reactive NP-specific CD8+ T cell responses, which correlated with protection against heterosubtypic H3N2 virus. The effect of TIV vaccination on TCR Vbeta-region bias of CD8+ T cells after secondary challenge with H3N2 virus was also investigated. These results suggest that suboptimal vaccination with conventional influenza vaccines may still positively modulate disease outcome, thereby allowing induction of heterosubtypic immunity by virus infection.
Published Version
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