PMID- 15207620
OWN - NLM
STAT- MEDLINE
DCOM- 20040730
LR  - 20191210
IS  - 0042-6822 (Print)
IS  - 0042-6822 (Linking)
VI  - 324
IP  - 2
DP  - 2004 Jul 1
TI  - A non-consensus branch point plays an important role in determining the stability 
      of the 2-kb LAT intron during acute and latent infections of herpes simplex virus 
      type-1.
PG  - 340-9
AB  - Herpes simplex virus type 1 (HSV-1) establishes lifelong latent infection in 
      sensory neurons of the peripheral nervous system. During HSV latency, the 
      latency-associated transcripts (LATs) are the only viral transcripts abundantly 
      expressed. The most abundant form of LATs is a 2-kb stable intron spliced from a 
      primary transcript (mLAT). It has been previously reported that a non-consensus 
      branch point influences the stability of the intron (in vitro) in cells 
      transfected with plasmid constructs (J. Virol. 71 (1997) 5849; J. Virol. 71 
      (1997) 4199). However, it is unknown whether this branch point is important in 
      determining LAT stability in vivo (in the context of virus). To study the role of 
      this stable intron in HSV-1 infection, we have constructed a mutant virus 
      KOS-CONS in which the branch point has been mutated to consensus branch point 
      nucleotides. The accumulation of the 2-kb intron in KOS-CONS-infected cells was 
      greatly reduced. The LAT intron was not detectable in KOS-CONS-infected mouse 
      trigeminal ganglia (TG) during acute and latent phase infection by Northern blot 
      analysis. Replication of the KOS-CONS and the wild-type KOS viruses on Vero cells 
      was determined to be similar, as was the level of HSV-1 DNA in mouse trigeminal 
      ganglia during acute and latent phase infection. Using the mouse TG explant 
      model, the reactivation pattern of both viruses was shown to be similar. Our data 
      suggest that the unique branch point plays a significant role in determining the 
      stability of LAT intron in vivo, but that the stability of the intron does not 
      appear to affect HSV-1 replication, the establishment of latency, or viral 
      reactivation.
FAU - Mukerjee, Ruma
AU  - Mukerjee R
AD  - Department of Microbiology, University of Pennsylvania Medical School, 315 
      Johnson Pavilion, Philadelphia, PA 19104-6076, USA.
FAU - Kang, Wen
AU  - Kang W
FAU - Suri, Vikram
AU  - Suri V
FAU - Fraser, Nigel W
AU  - Fraser NW
LA  - eng
GR  - NS 33768/NS/NINDS NIH HHS/United States
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Virology
JT  - Virology
JID - 0110674
RN  - 0 (DNA, Viral)
RN  - 0 (MicroRNAs)
RN  - 0 (RNA, Messenger)
RN  - 0 (Viral Proteins)
RN  - 0 (latency associated transcript, herpes simplex virus-1)
SB  - IM
MH  - Acute Disease
MH  - Animals
MH  - Chlorocebus aethiops
MH  - DNA, Viral/biosynthesis/genetics
MH  - Female
MH  - Herpes Simplex/*virology
MH  - Herpesvirus 1, Human/*genetics/growth & development
MH  - Introns/physiology
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - MicroRNAs
MH  - Point Mutation
MH  - RNA, Messenger/analysis/biosynthesis
MH  - Trigeminal Ganglion/virology
MH  - Vero Cells
MH  - Viral Proteins/biosynthesis/*genetics
MH  - Virus Latency/genetics
MH  - Virus Replication/genetics
EDAT- 2004/06/23 05:00
MHDA- 2004/07/31 05:00
CRDT- 2004/06/23 05:00
PHST- 2003/05/09 00:00 [received]
PHST- 2003/11/25 00:00 [revised]
PHST- 2004/03/24 00:00 [accepted]
PHST- 2004/06/23 05:00 [pubmed]
PHST- 2004/07/31 05:00 [medline]
PHST- 2004/06/23 05:00 [entrez]
AID - S0042682204002314 [pii]
AID - 10.1016/j.virol.2004.03.043 [doi]
PST - ppublish
SO  - Virology. 2004 Jul 1;324(2):340-9. doi: 10.1016/j.virol.2004.03.043.