A gammaherpesvirus-secreted activator of Vbeta4+ CD8+ T cells regulates chronic infection and immunopathology.

ABSTRACT: Little is known about herpesvirus modulation of T cell activation in latently infected individuals or the implications of such for chronic immune disorders. Murine gammaherpesvirus 68 (MHV68) elicits persistent activation of CD8(+) T cells bearing a Vbeta4(+) T cell receptor (TCR) by a completely unknown mechanism. We show that a novel MHV68 protein encoded by the M1 gene is responsible for Vbeta4(+) CD8(+) T cell stimulation in a manner reminiscent of a viral superantigen. During infection, M1 expression induces a Vbeta4(+) effector T cell response that resists functional exhaustion and appears to suppress virus reactivation from peritoneal cells by means of long-term interferon-gamma (IFNgamma) production. Mice lacking an IFNgamma receptor (IFNgammaR(-/-)) fail to control MHV68 replicati

SUBMITTER: Evans AG 

PROVIDER: S-EPMC2275388 | biostudies-literature | 2008 Mar

REPOSITORIES: biostudies-literature