PMID- 27618691
OWN - NLM
STAT- MEDLINE
DCOM- 20170926
LR  - 20190202
IS  - 1553-7374 (Electronic)
IS  - 1553-7366 (Print)
IS  - 1553-7366 (Linking)
VI  - 12
IP  - 9
DP  - 2016 Sep
TI  - Latency Entry of Herpes Simplex Virus 1 Is Determined by the Interaction of Its 
      Genome with the Nuclear Environment.
PG  - e1005834
LID - 10.1371/journal.ppat.1005834 [doi]
LID - e1005834
AB  - Herpes simplex virus 1 (HSV-1) establishes latency in trigeminal ganglia (TG) 
      sensory neurons of infected individuals. The commitment of infected neurons 
      toward the viral lytic or latent transcriptional program is likely to depend on 
      both viral and cellular factors, and to differ among individual neurons. In this 
      study, we used a mouse model of HSV-1 infection to investigate the relationship 
      between viral genomes and the nuclear environment in terms of the establishment 
      of latency. During acute infection, viral genomes show two major patterns: 
      replication compartments or multiple spots distributed in the nucleoplasm (namely 
      "multiple-acute"). Viral genomes in the "multiple-acute" pattern are 
      systematically associated with the promyelocytic leukemia (PML) protein in 
      structures designated viral DNA-containing PML nuclear bodies (vDCP-NBs). To 
      investigate the viral and cellular features that favor the acquisition of the 
      latency-associated viral genome patterns, we infected mouse primary TG neurons 
      from wild type (wt) mice or knock-out mice for type 1 interferon (IFN) receptor 
      with wt or a mutant HSV-1, which is unable to replicate due to the synthesis of a 
      non-functional ICP4, the major virus transactivator. We found that the inability 
      of the virus to initiate the lytic program combined to its inability to 
      synthesize a functional ICP0, are the two viral features leading to the formation 
      of vDCP-NBs. The formation of the "multiple-latency" pattern is favored by the 
      type 1 IFN signaling pathway in the context of neurons infected by a virus able 
      to replicate through the expression of a functional ICP4 but unable to express 
      functional VP16 and ICP0. Analyses of TGs harvested from HSV-1 latently infected 
      humans showed that viral genomes and PML occupy similar nuclear areas in infected 
      neurons, eventually forming vDCP-NB-like structures. Overall our study designates 
      PML protein and PML-NBs to be major cellular components involved in the control 
      of HSV-1 latency, probably during the entire life of an individual.
FAU - Maroui, Mohamed Ali
AU  - Maroui MA
AD  - Univ Lyon, Universite Claude Bernard Lyon 1, CNRS UMR 5310, INSERM U 1217, LabEx 
      DEVweCAN, Institut NeuroMyoGene (INMG), team Chromatin Assembly, Nuclear Domains, 
      Virus, Lyon, France.
FAU - Calle, Aleth
AU  - Calle A
AD  - Univ Lyon, Universite Claude Bernard Lyon 1, CNRS UMR 5310, INSERM U 1217, LabEx 
      DEVweCAN, Institut NeuroMyoGene (INMG), team Chromatin Assembly, Nuclear Domains, 
      Virus, Lyon, France.
FAU - Cohen, Camille
AU  - Cohen C
AD  - Univ Lyon, Universite Claude Bernard Lyon 1, CNRS UMR 5310, INSERM U 1217, LabEx 
      DEVweCAN, Institut NeuroMyoGene (INMG), team Chromatin Assembly, Nuclear Domains, 
      Virus, Lyon, France.
FAU - Streichenberger, Nathalie
AU  - Streichenberger N
AD  - Univ Lyon, Universite Claude Bernard Lyon 1, CNRS UMR 5310, INSERM U 1217, 
      Institut NeuroMyoGene (INMG), team Nerve-Muscle Interactions, Lyon, France.
AD  - Univ Lyon, Centre Hospitalier Universitaire de Lyon, Hospices Civils de Lyon, 
      Centre de Pathologie et Neuropathologie Est, Bron, France.
FAU - Texier, Pascale
AU  - Texier P
AD  - Univ Lyon, Universite Claude Bernard Lyon 1, CNRS UMR 5310, INSERM U 1217, LabEx 
      DEVweCAN, Institut NeuroMyoGene (INMG), team Chromatin Assembly, Nuclear Domains, 
      Virus, Lyon, France.
FAU - Takissian, Julie
AU  - Takissian J
AD  - Institut de Biologie Integrative de la Cellule (I2BC), Departement de Virologie, 
      Gif-sur-Yvette, France.
FAU - Rousseau, Antoine
AU  - Rousseau A
AD  - Institut de Biologie Integrative de la Cellule (I2BC), Departement de Virologie, 
      Gif-sur-Yvette, France.
AD  - Universite Paris Sud, Centre Hospitalier Universitaire de Bicetre, Service 
      d'Ophthalmologie, Le Kremlin-Bicetre, France.
FAU - Poccardi, Nolwenn
AU  - Poccardi N
AD  - Institut de Biologie Integrative de la Cellule (I2BC), Departement de Virologie, 
      Gif-sur-Yvette, France.
FAU - Welsch, Jeremy
AU  - Welsch J
AD  - Ecole Normale Superieure de Lyon, CNRS UMR 5308, INSERM U 1111, Centre 
      International de Recherche en Infectiologie (CIRI), team Immunobiologie des 
      infections virales, Lyon, France.
FAU - Corpet, Armelle
AU  - Corpet A
AD  - Univ Lyon, Universite Claude Bernard Lyon 1, CNRS UMR 5310, INSERM U 1217, LabEx 
      DEVweCAN, Institut NeuroMyoGene (INMG), team Chromatin Assembly, Nuclear Domains, 
      Virus, Lyon, France.
FAU - Schaeffer, Laurent
AU  - Schaeffer L
AD  - Univ Lyon, Universite Claude Bernard Lyon 1, CNRS UMR 5310, INSERM U 1217, 
      Institut NeuroMyoGene (INMG), team Nerve-Muscle Interactions, Lyon, France.
FAU - Labetoulle, Marc
AU  - Labetoulle M
AD  - Institut de Biologie Integrative de la Cellule (I2BC), Departement de Virologie, 
      Gif-sur-Yvette, France.
AD  - Universite Paris Sud, Centre Hospitalier Universitaire de Bicetre, Service 
      d'Ophthalmologie, Le Kremlin-Bicetre, France.
FAU - Lomonte, Patrick
AU  - Lomonte P
AD  - Univ Lyon, Universite Claude Bernard Lyon 1, CNRS UMR 5310, INSERM U 1217, LabEx 
      DEVweCAN, Institut NeuroMyoGene (INMG), team Chromatin Assembly, Nuclear Domains, 
      Virus, Lyon, France.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20160912
PL  - United States
TA  - PLoS Pathog
JT  - PLoS pathogens
JID - 101238921
RN  - 0 (Carrier Proteins)
RN  - 0 (Interferon Type I)
RN  - 0 (Pml protein, mouse)
RN  - 0 (Promyelocytic Leukemia Protein)
RN  - 0 (Trans-Activators)
RN  - 0 (Transcription Factors)
RN  - 156986-95-7 (Receptor, Interferon alpha-beta)
SB  - IM
CIN - Microb Cell. 2016 Nov 04;3(11):569-572. PMID: 28357326
MH  - Animals
MH  - Carrier Proteins/genetics/metabolism
MH  - Female
MH  - Genome, Viral/*genetics
MH  - Herpes Simplex/*virology
MH  - Herpesvirus 1, Human/*genetics/physiology
MH  - Humans
MH  - Interferon Type I/genetics/metabolism
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Mice, Knockout
MH  - Mutation
MH  - Promyelocytic Leukemia Protein/genetics/*metabolism
MH  - Receptor, Interferon alpha-beta/genetics/metabolism
MH  - Signal Transduction
MH  - Trans-Activators/genetics/metabolism
MH  - Transcription Factors/genetics/metabolism
MH  - Trigeminal Ganglion/virology
MH  - Virus Latency/*genetics
PMC - PMC5019400
COIS- The authors have declared that no competing interests exist.
EDAT- 2016/09/13 06:00
MHDA- 2017/09/28 06:00
PMCR- 2016/09/12
CRDT- 2016/09/13 06:00
PHST- 2016/04/12 00:00 [received]
PHST- 2016/07/30 00:00 [accepted]
PHST- 2016/09/13 06:00 [entrez]
PHST- 2016/09/13 06:00 [pubmed]
PHST- 2017/09/28 06:00 [medline]
PHST- 2016/09/12 00:00 [pmc-release]
AID - PPATHOGENS-D-16-00814 [pii]
AID - 10.1371/journal.ppat.1005834 [doi]
PST - epublish
SO  - PLoS Pathog. 2016 Sep 12;12(9):e1005834. doi: 10.1371/journal.ppat.1005834. 
      eCollection 2016 Sep.