Role of IL-22 during murine gammaherpesvirus infection
Description
Gammaherpesviruses are double-stranded DNA viruses that establish lifelong infections in over 95% of adults worldwide and are associated with multiple cancers and autoimmune disease. To persist within the host, these viruses exploit germinal center B cells to establish a long-lived latent reservoir. Although the cytokine IL-22 is best known for its protective role in bacterial and fungal infections, its contribution to gammaherpesvirus infection was unknown. Using a murine model of gammaherpesvirus infection, we demonstrate that IL-22 promotes the establishment of chronic gammaherpesvirus infection without affecting acute viral replication. Mice lacking IL-22 exhibited reduced latent viral burden accompanied by impaired germinal center and plasma-cell responses along with diminished virus-specific and polyclonal antibody production. These findings suggest that IL-22 helps create an immune environment that favors viral latency. Our work identifies a previously unrecognized role for IL-22 in supporting chronic gammaherpesvirus infection and provides new insights into how host immune pathways contribute to lifelong gammaherpesvirus infection.
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