Abstract
In recent years, it has been suggested that host cells exert intrinsic mechanisms to control nuclear replicating DNA viruses. This cellular response involves nuclear antiviral factors targeting incoming viral genomes. Herpes simplex virus-1 (HSV-1) is the best-studied model in this context, and it was shown that upon nuclear entry HSV-1 genomes are immediately targeted by components of promyelocytic leukemia nuclear bodies (PML-NBs) and the nuclear DNA sensor IFI16 (interferon gamma inducible protein 16). Based on HSV-1 studies, together with limited examples in other viral systems, these phenomena are widely believed to be a common cellular response to incoming viral genomes, although formal evidence for each virus is lacking. Indeed, recent studies suggest that the case may be different for adenovirus infection. Here we summarize the existing experimental evidence for the roles of nuclear antiviral factors against incoming viral genomes to better understand cellular responses on a virus-by-virus basis. We emphasize that cells seem to respond differently to different incoming viral genomes and discuss possible arguments for and against a unifying cellular mechanism targeting the incoming genomes of different virus families.
Highlights
Viruses are intracellular parasites and need to reach their site of replication in order to propagate; this requires overcoming several structural and molecular barriers of the host cell
SUMO-interacting motifs (SIMs)-like motifs in L2 and demonstrated that one of the SIM is critical for the binding of SUMO2 and the promyelocytic leukemia nuclear bodies (PML-NBs) targeting of L2 as well as viral genomes, contributing to efficient human papillomavirus (HPV) infection [32]
We tried to focus the attention of the reader on the existing experimental evidence as well as the possible explanations of how nuclear antiviral factors target incoming DNA viruses immediately upon infection
Summary
Viruses are intracellular parasites and need to reach their site of replication in order to propagate; this requires overcoming several structural and molecular barriers of the host cell. Largely from herpes simplex virus-1 (HSV-1) studies (see Section 3), have suggested that nuclear antiviral factors function as DNA sensors and effectors to target incoming viral genomes immediately upon nuclear entry [5]. This antiviral response by host nuclear factors is considered as a part of the “intrinsic immunity” [6,7] and may constitute a common mechanism against incoming genomes of nuclear replicating DNA viruses [5]. For cytoplasmic sensing of viruses or their genomes, please refer to several excellent reviews elsewhere [1,2,3]
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