Speaker
Description
The risk of emerging pandemic influenza A viruses (IAV) that approach the devastating 1918 strain motivates finding strain-specific host-pathogen mechanisms. During infection, dendritic cells (DC) mature into antigen-presenting cells that activate T cells, linking innate to adaptive immunity. DC infection with seasonal IAVs, but not with the 1918 and 2009 pandemic strains, induces global RNA degradation. Here we show that DC infection with seasonal IAV causes immunogenic RIPK3-mediated cell death. Pandemic IAV suppressed this immunogenic DC cell death. Only DC infected with seasonal IAV, but not with pandemic IAV, enhanced maturation of uninfected DC and T cell proliferation. In vivo, circulating T cell levels were reduced after a pandemic, but not seasonal, IAV infection. Using recombinant viruses, we identified the HA genomic segment as the mediator of cell death inhibition. These results identify a novel process of pandemic virus subversion of the immune response.
| Choose secondary Session | Virus host cell interaction |
|---|---|
| Choose primary session | Innate Immunity |
