PMID- 14610166
OWN - NLM
STAT- MEDLINE
DCOM- 20040105
LR  - 20190509
IS  - 0022-538X (Print)
IS  - 1098-5514 (Electronic)
IS  - 0022-538X (Linking)
VI  - 77
IP  - 23
DP  - 2003 Dec
TI  - Transgenic mouse with the herpes simplex virus type 1 latency-associated gene: 
      expression and function of the transgene.
PG  - 12421-9
AB  - During herpes simplex virus type 1 (HSV-1) latent infection in human peripheral 
      sensory ganglia, the major viral gene transcribed is the latency-associated 
      transcript (LAT) gene. In order to facilitate the study of this gene, we 
      generated a transgenic mouse that contains the DNA fragment that transcribes the 
      LAT RNAs (2.0 kb and its 1.5-kb spliced transcript) under control of the 
      cytomegalovirus promoter. The tissue distribution of these transcripts and their 
      effects upon HSV-1 replication, latency, and reactivation in the transgenic-mouse 
      model were examined. Different steady-state amounts of both transcripts were 
      found in various tissues. While the highest levels of the 2.0-kb RNA were 
      detected in heart and skeletal muscle, the 1.5-kb transcript was found at 
      elevated levels in the brain and at much higher levels in the trigeminal ganglia 
      (TG). Replication of both the wild-type and a LAT-negative mutant virus was 
      suppressed in primary embryonic fibroblasts obtained from LAT-expressing 
      transgenic mice compared to that in cells obtained from normal mice. HSV-1 DNA 
      amounts in latently infected TG of transgenic mice were similar to those in 
      normal mice. Reactivation of latent HSV-1 LAT-negative mutants by explant 
      cocultivation of TG from transgenic mice was more efficient than reactivation 
      from normal-mouse TG. Considering our present and previous results, we propose 
      that the significantly higher steady-state level of the 1.5-kb RNA in the TG may 
      link this transcript to latency functions and that by inhibition of virus 
      replication, the LAT gene may protect ganglion cells and thereby increase the 
      probability of reactivation.
FAU - Mador, Nurith
AU  - Mador N
AD  - Clinical Virology Unit, Laboratory of Neurovirology, Hadassah University 
      Hospital, Jerusalem, Israel.
FAU - Braun, Efrat
AU  - Braun E
FAU - Haim, Hillel
AU  - Haim H
FAU - Ariel, Ilana
AU  - Ariel I
FAU - Panet, Amos
AU  - Panet A
FAU - Steiner, Israel
AU  - Steiner I
LA  - eng
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 (DNA Primers)
RN  - 0 (DNA, Viral)
RN  - 0 (MicroRNAs)
RN  - 0 (RNA, Viral)
RN  - 0 (Viral Proteins)
RN  - 0 (latency associated transcript, herpes simplex virus-1)
SB  - IM
MH  - Animals
MH  - Base Sequence
MH  - DNA Primers
MH  - DNA, Viral/genetics
MH  - *Gene Expression
MH  - *Genes, Viral
MH  - Herpesvirus 1, Human/*genetics/physiology
MH  - Mice
MH  - Mice, Transgenic
MH  - MicroRNAs
MH  - RNA, Viral/genetics/metabolism
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - *Transgenes
MH  - Viral Proteins/*genetics
MH  - Virus Latency/*genetics
MH  - Virus Replication
PMC - PMC262558
EDAT- 2003/11/12 05:00
MHDA- 2004/01/06 05:00
PMCR- 2003/12/01
CRDT- 2003/11/12 05:00
PHST- 2003/11/12 05:00 [pubmed]
PHST- 2004/01/06 05:00 [medline]
PHST- 2003/11/12 05:00 [entrez]
PHST- 2003/12/01 00:00 [pmc-release]
AID - 0642 [pii]
AID - 10.1128/jvi.77.23.12421-12429.2003 [doi]
PST - ppublish
SO  - J Virol. 2003 Dec;77(23):12421-9. doi: 10.1128/jvi.77.23.12421-12429.2003.