DNA repair proteins affect the lifecycle of herpes simplex virus 1.
Ontology highlight
ABSTRACT: We report that herpes simplex virus 1 (HSV-1) infection can activate and exploit a cellular DNA damage response that aids viral replication in nonneuronal cells. Early in HSV-1 infection, several members of the cellular DNA damage-sensing machinery are activated and accumulate at sites of viral DNA replication. When this cellular response is abrogated, formation of HSV-1 replication centers is retarded, and viral production is compromised. In neurons, HSV-1 replication centers fail to mature, and the DNA damage response is not initiated. These data suggest that the failure of neurons to mount a DNA damage response to HSV-1 may contribute to the establishment of latency.
SUBMITTER: Lilley CE
PROVIDER: S-EPMC556126 | biostudies-literature |
REPOSITORIES: biostudies-literature
ACCESS DATA