Role of IL-22 during murine gammaherpesvirus infection

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.