PMID- 8799218
OWN - NLM
STAT- MEDLINE
DCOM- 19961114
LR  - 20191101
IS  - 1355-0284 (Print)
IS  - 1355-0284 (Linking)
VI  - 2
IP  - 4
DP  - 1996 Aug
TI  - A herpes simplex virus type 1 mutant with a deletion immediately upstream of the 
      LAT locus establishes latency and reactivates from latently infected mice with 
      normal kinetics.
PG  - 268-78
AB  - The latency associated transcripts (LATs) are the only abundant viral gene 
      products detected during latent herpes simplex virus (HSV) infection of 
      peripheral nerves in animals and people. A LAT promoter has been identified and 
      mutant viruses with lesions removing the promoter and surrounding region have 
      been observed to reactivate slowly from trigeminal ganglia (TG) explanted from 
      latently infected mice. Previous work has shown that most mutants with lesions 
      limited to regions downstream of the LAT promoter reactivate normally. Therefore, 
      to help map the boundaries of the slow reactivation phenotype, a mutant virus 
      with lesions located immediately upstream of the LAT promoter was constructed and 
      called 17 delta S/N. 17 delta S/N contains a 437 nucleotide (nt) deletion 332 nts 
      upstream of the TATAA box of the LAT promoter. In productively infected cells, 17 
      delta S/N failed to synthesize detectable amounts of the 1.1 and 1.8 kb 
      transcripts which are produced during wild-type infections and are specified by a 
      region just upstream of the LAT promoter. However, 17 delta S/N did produce 
      normal amounts of LAT in tissue culture as well as in neurons derived from 
      latently infected cells, as ascertained by Northern blot and in situ 
      hybridization analysis. Moreover, in latently infected mice, 17 delta S/N 
      established and maintained infection in as many neurons as did wild type virus, 
      as determined by in situ polymerase chain reaction (PCR) to detect viral DNA. 
      Finally, the virus reactivated from TG derived from latently infected mice with 
      kinetics indistinguishable from those of wild-type virus. Therefore, reactivation 
      from latency, in this model system, does not appear to require function from the 
      viral genomic region located immediately upstream of the LAT promoter.
FAU - Maggioncalda, J
AU  - Maggioncalda J
AD  - Jefferson Cancer Institute, Thomas Jefferson University, Philadelphia, 
      Pennsylvania 19107-6799, USA.
FAU - Mehta, A
AU  - Mehta A
FAU - Bagasra, O
AU  - Bagasra O
FAU - Fraser, N W
AU  - Fraser NW
FAU - Block, T M
AU  - Block TM
LA  - eng
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Neurovirol
JT  - Journal of neurovirology
JID - 9508123
RN  - 0 (DNA, Viral)
RN  - EC 3.1.21.- (endodeoxyribonuclease StyI)
RN  - EC 3.1.21.4 (Deoxyribonucleases, Type II Site-Specific)
RN  - EC 3.1.21.4 (GCGGCCGC-specific type II deoxyribonucleases)
SB  - IM
CIN - J Neurovirol. 1996 Aug;2(4):225-9. PMID: 8799212
MH  - Animals
MH  - Blotting, Northern
MH  - Blotting, Southern
MH  - Cells, Cultured/physiology/virology
MH  - Culture Techniques
MH  - DNA, Viral/genetics
MH  - Deoxyribonucleases, Type II Site-Specific
MH  - Female
MH  - *Gene Deletion
MH  - Genome, Viral
MH  - Genotype
MH  - Herpesviridae Infections/*genetics
MH  - Herpesvirus 1, Human/genetics/*physiology
MH  - Kinetics
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Mutation/physiology
MH  - Phenotype
MH  - Promoter Regions, Genetic/genetics
MH  - Transcription, Genetic/genetics
MH  - Trigeminal Ganglion/cytology/virology
MH  - *Virus Latency
EDAT- 1996/08/01 00:00
MHDA- 1996/08/01 00:01
CRDT- 1996/08/01 00:00
PHST- 1996/08/01 00:00 [pubmed]
PHST- 1996/08/01 00:01 [medline]
PHST- 1996/08/01 00:00 [entrez]
AID - 10.3109/13550289609146890 [doi]
PST - ppublish
SO  - J Neurovirol. 1996 Aug;2(4):268-78. doi: 10.3109/13550289609146890.