PMID- 10644361
OWN - NLM
STAT- MEDLINE
DCOM- 20000302
LR  - 20190508
IS  - 0022-538X (Print)
IS  - 1098-5514 (Electronic)
IS  - 0022-538X (Linking)
VI  - 74
IP  - 4
DP  - 2000 Feb
TI  - The latency-associated transcript gene enhances establishment of herpes simplex 
      virus type 1 latency in rabbits.
PG  - 1885-91
AB  - The latency-associated transcript (LAT) gene the only herpes simplex virus type 1 
      (HSV-1) gene abundantly transcribed during neuronal latency, is essential for 
      efficient in vivo reactivation. Whether LAT increases reactivation by a direct 
      effect on the reactivation process or whether it does so by increasing the 
      establishment of latency, thereby making more latently infected neurons available 
      for reactivation, is unclear. In mice, LAT-negative mutants appear to establish 
      latency in fewer neurons than does wild-type HSV-1. However, this has not been 
      confirmed in the rabbit, and the role of LAT in the establishment of latency 
      remains controversial. To pursue this question, we inserted the gene for the 
      enhanced green fluorescent protein (EGFP) under control of the LAT promoter in a 
      LAT-negative virus (DeltaLAT-EGFP) and in a LAT-positive virus (LAT-EGFP). Sixty 
      days after ocular infection, trigeminal ganglia (TG) were removed from the 
      latently infected rabbits, sectioned, and examined by fluorescence microscopy. 
      EGFP was detected in significantly more LAT-EGFP-infected neurons than 
      DeltaLAT-EGFP-infected neurons (4.9% versus 2%, P < 0.0001). The percentages of 
      EGFP-positive neurons per TG ranged from 0 to 4.6 for DeltaLAT-EGFP and from 2.5 
      to 11.1 for LAT-EGFP (P = 0.003). Thus, LAT appeared to increase neuronal latency 
      in rabbit TG by an average of two- to threefold. These results suggest that LAT 
      enhances the establishment of latency in rabbits and that this may be one of the 
      mechanisms by which LAT enhances spontaneous reactivation. These results do not 
      rule out additional LAT functions that may be involved in maintenance of latency 
      and/or reactivation from latency.
FAU - Perng, G C
AU  - Perng GC
AD  - Ophthalmology Research Laboratories, Cedars-Sinai Medical Center Burns & Allen 
      Research Institute, Los Angeles, California 90048, USA.
FAU - Slanina, S M
AU  - Slanina SM
FAU - Yukht, A
AU  - Yukht A
FAU - Ghiasi, H
AU  - Ghiasi H
FAU - Nesburn, A B
AU  - Nesburn AB
FAU - Wechsler, S L
AU  - Wechsler SL
LA  - eng
GR  - EY07566/EY/NEI NIH HHS/United States
GR  - EY10243/EY/NEI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Virol
JT  - Journal of virology
JID - 0113724
RN  - 0 (Luminescent Proteins)
RN  - 147336-22-9 (Green Fluorescent Proteins)
SB  - IM
MH  - Animals
MH  - Gene Expression Regulation
MH  - *Genes, Viral
MH  - Green Fluorescent Proteins
MH  - Herpesvirus 1, Human/*genetics/physiology
MH  - Humans
MH  - Luminescent Proteins/genetics
MH  - Neurons/virology
MH  - *Promoter Regions, Genetic
MH  - Rabbits
MH  - Trigeminal Ganglion/virology
MH  - *Virus Latency
MH  - Virus Replication
PMC - PMC111666
EDAT- 2000/01/22 09:00
MHDA- 2000/03/04 09:00
PMCR- 2000/02/01
CRDT- 2000/01/22 09:00
PHST- 2000/01/22 09:00 [pubmed]
PHST- 2000/03/04 09:00 [medline]
PHST- 2000/01/22 09:00 [entrez]
PHST- 2000/02/01 00:00 [pmc-release]
AID - 1609 [pii]
AID - 10.1128/jvi.74.4.1885-1891.2000 [doi]
PST - ppublish
SO  - J Virol. 2000 Feb;74(4):1885-91. doi: 10.1128/jvi.74.4.1885-1891.2000.