Figure 1.

Nuclear functions of non-essential HSV-1 proteins. HSV-1 encodes multiple proteins able to counteract antiviral host responses within the nucleus. (A): ICP0 functions as an E3 ligase ubiquitin ligase that degrades ND10 components that encapsulate the viral genome in the nucleus, including PML, Daxx, SP100, centromeric proteins, and others. The degradation of IFI16 involves multiple factors. These events facilitate initiation of viral gene transcription. (B): The viral protein ICP0 is also known to disrupt repressor complexes that silence the viral genome, as well as recruit factors to enable viral gene transcription. Altogether, ICP0 facilitates permissive histone modifications, while suppressing silencing modifications, to enable for viral gene expression. (C): The viral kinases U_S3 and U_L13, with ICP22, are known to facilitate viral late gene expression, which occurs through the recruitment of host factors, such as Topoisomerase IIα and RNA polymerase II, to the sites of DNA replication in the nucleus. Together, these non-essential viral proteins are important for optimal expression of other viral genes and for viral DNA replication.