PMID- 16940542
OWN - NLM
STAT- MEDLINE
DCOM- 20061020
LR  - 20220311
IS  - 0022-538X (Print)
IS  - 1098-5514 (Electronic)
IS  - 0022-538X (Linking)
VI  - 80
IP  - 18
DP  - 2006 Sep
TI  - Herpes simplex virus type 1 latently infected neurons differentially express 
      latency-associated and ICP0 transcripts.
PG  - 9310-21
AB  - During the latent phase of herpes simplex virus type 1 (HSV-1) infection, the 
      latency-associated transcripts (LATs) are the most abundant viral transcripts 
      present in neurons, but some immediate-early viral transcripts, such as those 
      encoding ICP0, have also been reported to be transcribed in latently infected 
      mouse trigeminal ganglia (TG). A murine oro-ocular model of herpetic infection 
      was used to study ICP0 gene expression in the major anatomical sites of HSV-1 
      latency, including the TG, superior cervical ganglion, spinal cord, and 
      hypothalamus. An HSV-1 recombinant strain, SC16 110LacZ, revealed ICP0 promoter 
      activity in several neurons in latently infected ganglia, and following infection 
      with wild-type HSV-1 strain SC16, in situ hybridization analyses identified ICP0 
      transcripts in the nuclei of neurons at times consistent with the establishment 
      of latency. Reverse transcription (RT)-PCR assays performed on RNA extracted from 
      latently infected tissues indicated that ICP0 transcripts were detected in all 
      anatomical sites of viral latency. Furthermore, quantitative real-time RT-PCR 
      showed that neurons differentially expressed the LATs and ICP0 transcripts, with 
      splicing of ICP0 transcripts being dependent on the anatomical location of 
      latency. Finally, TG neurons were characterized by high-level expression of LATs 
      and detection of abundant unspliced ICP0 transcripts, a pattern markedly 
      different from those of other anatomical sites of HSV-1 latency. These results 
      suggest that LATs might be involved in the maintenance of HSV-1 latency through 
      the posttranscriptional regulation of ICP0 in order to inhibit expression of this 
      potent activator of gene expression during latency.
FAU - Maillet, Severine
AU  - Maillet S
AD  - Laboratoire de Virologie Moleculaire et Structurale, Centre National de la 
      Recherche Scientifique, 91198 Gif-sur-Yvette, France. marc.labetoulle@bct.aphp.fr
FAU - Naas, Thierry
AU  - Naas T
FAU - Crepin, Sophie
AU  - Crepin S
FAU - Roque-Afonso, Anne-Marie
AU  - Roque-Afonso AM
FAU - Lafay, Florence
AU  - Lafay F
FAU - Efstathiou, Stacey
AU  - Efstathiou S
FAU - Labetoulle, Marc
AU  - Labetoulle M
LA  - eng
GR  - G9800943/MRC_/Medical Research Council/United Kingdom
GR  - WT_/Wellcome Trust/United Kingdom
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Virol
JT  - Journal of virology
JID - 0113724
RN  - 0 (Immediate-Early Proteins)
RN  - 0 (RNA, Messenger)
RN  - EC 2.3.2.27 (Ubiquitin-Protein Ligases)
RN  - EC 2.3.2.27 (Vmw110 protein, Human herpesvirus 1)
SB  - IM
MH  - Animals
MH  - Brain/virology
MH  - Female
MH  - *Gene Expression Regulation, Viral
MH  - Herpesvirus 1, Human/*metabolism
MH  - Humans
MH  - Immediate-Early Proteins/*biosynthesis/chemistry
MH  - Introns
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Neurons/*virology
MH  - RNA Splicing
MH  - RNA, Messenger/metabolism
MH  - Ubiquitin-Protein Ligases/*biosynthesis/chemistry
PMC - PMC1563928
EDAT- 2006/08/31 09:00
MHDA- 2006/10/21 09:00
PMCR- 2007/01/01
CRDT- 2006/08/31 09:00
PHST- 2006/08/31 09:00 [pubmed]
PHST- 2006/10/21 09:00 [medline]
PHST- 2006/08/31 09:00 [entrez]
PHST- 2007/01/01 00:00 [pmc-release]
AID - 80/18/9310 [pii]
AID - 2615-05 [pii]
AID - 10.1128/JVI.02615-05 [doi]
PST - ppublish
SO  - J Virol. 2006 Sep;80(18):9310-21. doi: 10.1128/JVI.02615-05.