Abstract
Herpesviruses are important pathogens that can cause significant morbidity and mortality in the human population. Herpesviruses have a double-stranded DNA genome, and viral genome replication takes place inside the nucleus. Upon entering the nucleus, herpesviruses have to overcome the obstacle of cellular proteins in order to enable viral gene expression and genome replication. In this review, we want to highlight cellular proteins that sense incoming viral genomes of the DNA-damage repair (DDR) pathway and of PML-nuclear bodies (PML-NBs) that all can act as antiviral restriction factors within the first hours after the viral genome is released into the nucleus. We show the function and significance of both nuclear DNA sensors, the DDR and PML-NBs, and demonstrate for three human herpesviruses of the alpha-, beta- and gamma-subfamilies, HSV-1, HCMV and KSHV respectively, how viral tegument proteins antagonize these pathways.
Highlights
Herpesviruses have evolved sophisticated ways to subvert the immune system over millions of years of coevolution with their respective hosts
While herpesviruses need to surmount adaptive cell-mediated immunity in order to prevent being killed by immune cells and establish persistent infection, the antagonism of cellular restriction and the innate immune system is of particular importance in order to achieve efficient infection of target cells
A hallmark of herpesvirus infections is the establishment of lifelong latency [1]; for example, about 3.7 billion people are infected with HSV-1 worldwide [2], and even more by HHV-6, -7, and Epstein-Barr virus (EBV) [3,4]
Summary
Herpesviruses have evolved sophisticated ways to subvert the immune system over millions of years of coevolution with their respective hosts. A hallmark of herpesvirus infections is the establishment of lifelong latency [1]; for example, about 3.7 billion people are infected with HSV-1 worldwide [2], and even more by HHV-6, -7, and EBV [3,4]. In this regard, herpesviruses are the most “successful” virus family in the human population, because almost all human adults are latently infected with at least one herpesvirus, and most by several. We want to demonstrate how herpesviral proteins, in particular tegument proteins that enter the cell as part of the viral particle, antagonize cellular restriction factors
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