Evasion of adaptive and innate immune response mechanisms by γ-herpesviruses

Abstract

γ-Herpesviral immune evasion mechanisms are optimized to support the acute, lytic and the longterm, latent phase of infection. During acute infection, specific immune modulatory proteins limit, but also exploit, the antiviral activities of cell intrinsic innate immune responses as well as those of innate and adaptive immune cells. During latent infection, a restricted gene expression program limits immune targeting and cis-acting mechanisms to reduce the antigen presentation as well as antigenicity of latency-associated proteins. Here, we will review recent progress in our understanding of γ-herpesviral immune evasion strategies.

Figure 1

Evasion of T cell responses by g herpesviruses.

Figure 2

Inhibition of the classical apoptosis and autophagy pathway by γ-herpesvirus proteins. KSHV vFLIP and K7 target pro-caspase 8 and activated caspase 3 for inhibition, whereas vBcl2 and MHV-68 vMAP antagonize the oligomerization of Bax/Bak and VDAC that release cytochrome c (cyto. c). Additionally, KSHV K7 activates CAML in releasing calcium from the ER to attenuate stress induced apoptosis. Of the classic autophagy pathway, vBcl2 suppresses UVRAG in autophagosome formation. Viral proteins are colored in green.