Abstract
The MHC class I presentation is responsible for the presentation of viral proteins to CD8+ T lymphocytes and mainly depends on the classical antigen processing pathway. Recently, a second pathway involving autophagy has been implicated in this process. Here, we show an increase in the capacity of murine dendritic cells (DCs) to present viral antigens on MHC class I after infection with a mutant herpes simplex virus 1 (HSV-1-Δ34.5), lacking infected cell protein 34.5 (ICP34.5), when compared to its parental HSV-1 strain. The ICP34.5 protein counteracts host cell translational arrest and suppresses macroautophagy, and the lack of this protein resulted in a low viral protein abundance, which was processed and presented in an efficient way. Our study demonstrates an important role of autophagy in processing endogenous viral proteins in HSV-1-infected DCs.