PMID- 9445025
OWN - NLM
STAT- MEDLINE
DCOM- 19980218
LR  - 20240214
IS  - 0022-538X (Print)
IS  - 1098-5514 (Electronic)
IS  - 0022-538X (Linking)
VI  - 72
IP  - 2
DP  - 1998 Feb
TI  - Use of differential display reverse transcription-PCR to reveal cellular changes 
      during stimuli that result in herpes simplex virus type 1 reactivation from 
      latency: upregulation of immediate-early cellular response genes TIS7, 
      interferon, and interferon regulatory factor-1.
PG  - 1252-61
AB  - The detailed mechanism which governs the choice between herpes simplex virus 
      (HSV) latency and reactivation remains to be elucidated. It is probable that 
      altered expression of cellular factors in sensory neurons leads to induction of 
      HSV gene expression resulting in reactivation. As an approach to identify novel 
      cellular genes which are activated or repressed by stimuli that reactivate HSV 
      from latency and hence may play a role in viral reactivation, RNA from explanted 
      trigeminal ganglia (TG) was analyzed by differential display reverse 
      transcription-PCR (DDRT-PCR). Nearly 50 cDNAs whose mRNA level was modified by 
      the stress of explantation were isolated and sequenced. We present a listing of a 
      spectrum of altered RNAs, including both known and unknown sequences. Five of 
      those differentially displayed transcripts were identified as interferon-related 
      murine TIS7 mRNA. These results were confirmed in both infected and uninfected 
      ganglia by quantitative RNase protection assay and immunostaining. Alpha and beta 
      interferons and interferon regulatory factor-1 (IRF-1) were also induced by 
      explantation. In addition, we have identified sequences that correspond to IRF-1 
      consensus binding sites in both HSV type 1 origins of replication. Our findings 
      suggest that physiological pathways that include these cellular factors may be 
      involved in modulating HSV reactivation.
FAU - Tal-Singer, R
AU  - Tal-Singer R
AD  - The Wistar Institute, Philadelphia, Pennsylvania 19104-4268, USA.
FAU - Podrzucki, W
AU  - Podrzucki W
FAU - Lasner, T M
AU  - Lasner TM
FAU - Skokotas, A
AU  - Skokotas A
FAU - Leary, J J
AU  - Leary JJ
FAU - Fraser, N W
AU  - Fraser NW
FAU - Berger, S L
AU  - Berger SL
LA  - eng
GR  - NS33768/NS/NINDS NIH HHS/United States
GR  - CA09171/CA/NCI NIH HHS/United States
GR  - P50 NS033768/NS/NINDS NIH HHS/United States
GR  - T32 CA009171/CA/NCI NIH HHS/United States
GR  - P01 NS033768/NS/NINDS 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 (DNA-Binding Proteins)
RN  - 0 (IFRD1 protein, human)
RN  - 0 (Ifrd1 protein, mouse)
RN  - 0 (Immediate-Early Proteins)
RN  - 0 (Interferon Regulatory Factor-1)
RN  - 0 (Irf1 protein, mouse)
RN  - 0 (Membrane Proteins)
RN  - 0 (Phosphoproteins)
RN  - 9008-11-1 (Interferons)
SB  - IM
MH  - Animals
MH  - Base Sequence
MH  - DNA-Binding Proteins/biosynthesis/*genetics
MH  - *Gene Expression Regulation, Viral
MH  - Genes, Tumor Suppressor
MH  - Herpesvirus 1, Human/*physiology
MH  - Immediate-Early Proteins/biosynthesis/*genetics
MH  - Interferon Regulatory Factor-1
MH  - Interferons/biosynthesis/*genetics
MH  - Membrane Proteins/biosynthesis/*genetics
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Molecular Sequence Data
MH  - Phosphoproteins/biosynthesis/*genetics
MH  - Polymerase Chain Reaction/*methods
MH  - Up-Regulation
MH  - Virus Activation/*genetics
MH  - Virus Latency
PMC - PMC124603
EDAT- 1998/01/28 00:00
MHDA- 1998/01/28 00:01
PMCR- 1998/02/01
CRDT- 1998/01/28 00:00
PHST- 1998/01/28 00:00 [pubmed]
PHST- 1998/01/28 00:01 [medline]
PHST- 1998/01/28 00:00 [entrez]
PHST- 1998/02/01 00:00 [pmc-release]
AID - 1367 [pii]
AID - 10.1128/JVI.72.2.1252-1261.1998 [doi]
PST - ppublish
SO  - J Virol. 1998 Feb;72(2):1252-61. doi: 10.1128/JVI.72.2.1252-1261.1998.