T cell immunity in HSV-1-and VZV-infected neural ganglia

Herpesviruses hijack the MHC class I (MHC I) and class II (MHC II) antigen -pre-sentation pathways to manipulate immune recognition by T cells. First, we illus-trate herpes simplex virus-1 (HSV-1) and varicella-zoster virus (VZV) MHC immune evasion strategies. Next, we describe MHC-T cell interactions in HSV-1-and VZV-infected neural ganglia. Although studies on the topic are scarce, and use different models, most reports indicate that neuronal HSV-1 in-fection is mainly controlled by CD8+ T cells through noncytolytic mechanisms, whereas VZV seems to be largely controlled through CD4+ T cell-specific immune responses. Autologous human stem-cell-derived in vitro models could substantially aid in elucidating these neuroimmune interactions and are fit for studies on both herpesviruses.

Automated summary

Herpesviruses manipulate immune recognition by T cells through hijacking the MHC I and MHC II antigen presentation pathways. The MHC immune evasion strategies of herpes simplex virus-1 (HSV-1) and varicella-zoster virus (VZV) are illustrated. MHC-T cell interactions in HSV-1 and VZV-infected neural ganglia are described, with CD8+ T cells playing a major role in controlling neuronal HSV-1 infection and CD4+ T cells being important in controlling VZV infection. Autologous human stem-cell-derived in vitro models provide valuable tools for studying these neuroimmune interactions.