HSV-1 Genome Subnuclear Positioning and Associations with Host-Cell PML-NBs and Centromeres Regulate LAT Locus Transcription during Latency in Neurons

Major human pathologies are caused by nuclear replicative viruses establishing life-long latent infection in their host. during latency the genomes of these viruses are intimately interacting with the cell nucleus environment. a hallmark of herpes simplex virus type 1 (hsv-1) latency establishment is the shutdown of lytic genes expression and the concomitant induction of the latency associated (lat) transcripts. although the setting up and the maintenance of the latent genetic program is most likely dependent on a subtle interplay between viral and nuclear factors,this remains uninvestigated. combining the use of in situ fluorescent-based approaches and high-resolution microscopic analysis,we show that hsv-1 genomes adopt specific nuclear patterns in sensory neurons of latently infected mice (28 days post-inoculation,d.p.i.). latent hsv-1 genomes display two major patterns,called single and multiple