PMID- 21325410
OWN - NLM
STAT- MEDLINE
DCOM- 20110614
LR  - 20211020
IS  - 1098-5514 (Electronic)
IS  - 0022-538X (Print)
IS  - 0022-538X (Linking)
VI  - 85
IP  - 9
DP  - 2011 May
TI  - Herpes simplex virus 2 microRNA miR-H6 is a novel latency-associated 
      transcript-associated microRNA, but reduction of its expression does not 
      influence the establishment of viral latency or the recurrence phenotype.
PG  - 4501-9
LID - 10.1128/JVI.01997-10 [doi]
AB  - The herpes simplex virus 2 (HSV-2) viral microRNA (miRNA) designated miR-H6 is 
      located upstream of the latency-associated transcript (LAT) promoter region on 
      the strand opposite the LAT. Deletion of the LAT promoter and part of LAT exon 1 
      abolished HSV-2 miR-H6 expression in acutely and latently infected guinea pig 
      dorsal root ganglia (DRG), suggesting that this region is needed both for the 
      expression of LAT-encoded miRNAs and for miR-H6 expression in vivo. Relative to 
      cells infected with a viral rescuant, miR-H6 expression was significantly reduced 
      in cells infected with a mutant HSV-2 virus, NotPolyA, with an insertion of a 
      simian virus (SV40) polyadenylation signal sequence between the LAT promoter and 
      miR-H6 sequences. In addition, expression of miR-H6, but not LAT or viral DNA, 
      was significantly reduced in both mouse trigeminal ganglia (TG) and guinea pig 
      DRG latently infected with the NotPolyA mutant. Guinea pigs infected with 
      NotPolyA experienced reduced neurological complications of acute infection 
      relative to those infected with the rescuant, but the recurrence phenotype of the 
      NotPolyA mutant was similar to those of its rescuant and wild-type HSV-2, 
      indicating that reduction of miR-H6 expression is not by itself able to alter the 
      establishment of latency for the wild-type virus or the recurrence phenotype. 
      Furthermore, the mutation in NotPolyA did not affect the propensity of wild-type 
      HSV-2 to establish latency in neurons positive for subtype marker KH10. In 
      contrast to published reports regarding its HSV-1 homolog, HSV-2 miR-H6 did not 
      affect ICP4 expression in transfected or infected cells. We hypothesize that 
      viral miRNAs associated with LAT expression are likely to work collectively, 
      contributing to the phenotype attributed to the LAT.
FAU - Tang, Shuang
AU  - Tang S
AD  - Division of Viral Products, Office of Vaccines Research and Review, Center for 
      Biologics Evaluation and Research, Food and Drug Administration, Bethesda, 
      Maryland 20892, USA.
FAU - Bertke, Andrea S
AU  - Bertke AS
FAU - Patel, Amita
AU  - Patel A
FAU - Margolis, Todd P
AU  - Margolis TP
FAU - Krause, Philip R
AU  - Krause PR
LA  - eng
GR  - Intramural NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Intramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20110216
PL  - United States
TA  - J Virol
JT  - Journal of virology
JID - 0113724
RN  - 0 (LAT protein, Human herpesvirus 2)
RN  - 0 (MicroRNAs)
RN  - 0 (RNA, Viral)
RN  - 0 (Viral Proteins)
SB  - IM
MH  - Animals
MH  - Female
MH  - Ganglia, Spinal/virology
MH  - *Gene Expression Regulation, Viral
MH  - Guinea Pigs
MH  - Herpesvirus 2, Human/genetics/*physiology
MH  - Mice
MH  - MicroRNAs/*metabolism
MH  - RNA, Viral/*metabolism
MH  - Viral Proteins/biosynthesis/genetics
MH  - *Virus Latency
PMC - PMC3126258
EDAT- 2011/02/18 06:00
MHDA- 2011/06/15 06:00
PMCR- 2011/11/01
CRDT- 2011/02/18 06:00
PHST- 2011/02/18 06:00 [entrez]
PHST- 2011/02/18 06:00 [pubmed]
PHST- 2011/06/15 06:00 [medline]
PHST- 2011/11/01 00:00 [pmc-release]
AID - JVI.01997-10 [pii]
AID - 1997-10 [pii]
AID - 10.1128/JVI.01997-10 [doi]
PST - ppublish
SO  - J Virol. 2011 May;85(9):4501-9. doi: 10.1128/JVI.01997-10. Epub 2011 Feb 16.