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Genomes nuclear positioning to control transcriptional activity of herpes simplex virus 1. The role of promyelocytic leukemia nuclear bodies

Genomes nuclear positioning to control transcriptional activity of herpes simplex virus 1. The role of promyelocytic leukemia nuclear bodies

 

Patrick Lomonte

 

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-69008, Lyon, France

 

The comprehension of the molecular mechanisms contributing to the persistence of a virus in its host is essential to be able to design new therapies to control viral reactivation and the associated diseases. Herpes simplex virus 1 (HSV-1) is a DNA virus and a major human pathogen that remains latent as an unintegrated episome in the nucleus of neurons of the peripheral and central nervous systems of the infected host. The latency is unstable, and frequent symptomatic and asymptomatic reactivations of the virus are responsible for PNS and CNS pathologies. It is thus crucial to understand the physiological, immunological and molecular levels of interplay between latent HSV-1 and the host. Promyelocytic leukemia nuclear bodies (PML NBs, also called ND10) are known for their implication in multiple cell processes among other apoptosis, senescence and aging, but also as nuclear sensors of multiple stresses including viral infections. During these last years, my team demonstrated a major role of PML NBs in favoring the establishment of a latent state for HSV-1. A hallmark of HSV-1 latency establishment is the formation of PML NBs containing viral genomes, which we called viral DNA-containing PML NBs (vDCP NBs). The HSV-1 genomes entrapped in the vDCP NBs are transcriptionally silenced. This naturally occurring latent/quiescent state can be transcriptionally reactivated provided that vDCP NBs are destabilized, meaning that the latent virus is not definitively silent. Part of the PML/vDCP NBs associated transcriptional silencing is due to PML-dependent specific viral genomes chromatinization. During my talk I will give an overview of the involvement of the PML/vDCP NBs in controlling HSV-1 latency through epigenetic regulations by viral genomes nuclear positioning and chromatin marks apposition. I will also discuss about the similarities at the molecular level among (i) vDCP NBs, (ii) telomeres-containing ALT-associated PML NBs (APBs) present in telomerase negative cancer cells, and pericentromeres-containing giant PML NBs formed in cells from patients suffering of the Immunodeficiency, Centromeric instability, Facial anomalies (ICF) genetic syndrome.

 

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