title: The interaction between herpes simplex virus 1 genome and promyelocytic leukemia nuclear bodies (PML-NBs) as a hallmark of the entry in latency.
abstract: Herpes simplex virus 1 (HSV-1) is a human pathogen that establishes latency in the nucleus of infected neurons in the PNS and the CNS. At the transcriptional level latency is characterized by aquasi-complete silencing of the extrachromosomal viral genome that otherwise expresses more than 80 genes during the lytic cycle. In neurons, latency is anticipated to be the default transcriptional program; however, limited information exists on the molecular mechanisms that force the virus to enter the latent state. Our recent study demonstrates that the interaction of the viral genomes with the nuclear architecture and specifically the promyelocytic leukemia nuclear bodies (PML-NBs) is a major determinant for the entry of HSV-1 into latency (Maroui MA, Callé Aet al. (2016). Latency entry of herpes simplex virus 1 is determined by the interaction of its genome with the nuclear environment. PLoS Pathogens 12(9): e1005834.).
authors.affiliation: Univ Lyon, Université Claude Bernard Lyon 1, CNRS UMR 5310, INSERM U 1217, LabEx, DEVweCAN, Institut NeuroMyoGène (INMG), team Chromatin Assembly, Nuclear Domains, Virus; F-69100, Lyon, France.
authors.forename: Patrick
authors.initials: P
authors.lastname: Lomonte
keywords: Herpesvirus; herpes simplex virus 1 (HSV-1); intrinsic immunity; latency; neurons; nuclear architecture; promyelocytic leukemia nuclear bodies (PML-NBs)