Regulation of the innate immune response in human neurons by ICP34.5 maintains herpes simplex virus 1 latency.

ABSTRACT: Herpes simplex virus 1 (HSV-1) establishes latent infections in sensory neurons, from which HSV sporadically reactivates due to external stress and other stimuli. Latency and reactivation are studied through in vivo models in a variety of hosts, as well as in vitro models using primary neurons, and neurons derived from pluripotent stem cells (iPSCs). These systems behave disparately, but the reasons remain unknown. The interferon (IFN)-based neuronal innate immune response is critical in controlling HSV-1 replication and HSV-1 counters these responses in part through infected-cell protein 34.5 (ICP34.5). ICP34.5 also promotes neurovirulence by preventing host translational shutoff and interfering with host cell autophagy. Here we demonstrate in a human iPSC neuronal model tha

SUBMITTER: Canova PN 

PROVIDER: S-EPMC12026746 | biostudies-literature | 2025 Apr

REPOSITORIES: biostudies-literature