The interaction between herpes simplex virus 1 genome and promyelocytic leukemia nuclear bodies (PML-NBs) as a hallmark of the entry in latency
Authors:Patrick Lomonte
doi: 10.15698/mic2016.11.541
Volume 3, pp. 569 to 572, published 04/11/2016.
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.
Keywords:
Herpesvirus, herpes simplex virus 1 (HSV-1), latency, neurons, nuclear architecture, promyelocytic leukemia nuclear bodies (PML-NBs), intrinsic immunity.
Corresponding Author(s):
Conflict of interest statement:
The author declares no conflict of interest.
Please cite this article as:
Patrick Lomonte (2016). The interaction between herpes simplex virus 1 genome and promyelocytic leukemia nuclear bodies (PML-NBs) as a hallmark of the entry in latency. Microbial Cell 3(11): 569-572. doi: 10.15698/mic2016.11.541
© 2016 Lomonte. This is an open-access article released under the terms of the Creative Commons Attribution (CC BY) license, which allows the unrestricted use, distribution, and reproduction in any medium, provided the original author and source are acknowledged.
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 a quasi-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 A et 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.).