PMID- 11483762
OWN - NLM
STAT- MEDLINE
DCOM- 20010906
LR  - 20190508
IS  - 0022-538X (Print)
IS  - 1098-5514 (Electronic)
IS  - 0022-538X (Linking)
VI  - 75
IP  - 17
DP  - 2001 Sep
TI  - The 2.2-kilobase latency-associated transcript of herpes simplex virus type 2 
      does not modulate viral replication, reactivation, or establishment of latency in 
      transgenic mice.
PG  - 8166-72
AB  - To better understand the mechanisms responsible for the observed effects of 
      deletions in the promoter region of the latency-associated transcript (LAT) gene 
      in impairing herpes simplex virus (HSV) reactivation, we generated mice 
      transgenic for a 5.5-kb HSV type 2 (HSV-2) genomic fragment spanning the major 
      LAT, along with the LAT promoter and flanking regions, in the C57BL/6 background. 
      The mice expressed abundant 2.2-kb major LATs in trigeminal ganglia (TG) and 
      other tissues. The effects of the transgene on HSV-2 infection, latency, and 
      reactivation were assessed. When infected with wild-type (WT) HSV-2 or its LAT 
      promoter deletion (LAT(-)) mutant, primary lung fibroblast lines established from 
      normal C57BL/6 and transgenic mice supported virus growth equally well. The 
      replication of these viruses in the mouse eye and their spread to TG and brains 
      were similar. The quantities of latent viral DNA in TG of transgenic and normal 
      mice, as determined by real-time PCR, were comparable. UV light-induced 
      reactivation of the LAT(-) mutant from transgenic mice (0 to 7%) was no more 
      frequent than that from normal mice (0 to 14%), while WT virus was reactivated 
      from 13 to 54% of normal mice and 22 to 54% of transgenic mice. The cumulative 
      data indicate that, when expressed transgenically, the HSV-2 major LAT cannot 
      influence HSV-2 infection or latency and cannot complement the defect in 
      reactivation of the LAT(-) mutant. These results imply that the phenotype of 
      reduced reactivation associated with the LAT(-) mutant is related to a function 
      encoded in the LAT promoter but not to the major LAT itself.
FAU - Wang, K
AU  - Wang K
AD  - Medical Virology Section, Laboratory of Clinical Investigation, National 
      Institute of Allergy and Infectious Diseases, Bethesda, Maryland 20892, USA. 
      kwang@niaid.nih.gov
FAU - Pesnicak, L
AU  - Pesnicak L
FAU - Guancial, E
AU  - Guancial E
FAU - Krause, P R
AU  - Krause PR
FAU - Straus, S E
AU  - Straus SE
LA  - eng
PT  - Journal Article
PL  - United States
TA  - J Virol
JT  - Journal of virology
JID - 0113724
SB  - IM
MH  - Animals
MH  - Brain/virology
MH  - Cells, Cultured
MH  - Eye/virology
MH  - Fibroblasts
MH  - *Gene Expression Regulation, Viral
MH  - Herpesvirus 2, Human/genetics/isolation & purification/*physiology
MH  - Keratitis, Herpetic/*virology
MH  - Lung/cytology
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Transgenic
MH  - Transgenes
MH  - Trigeminal Ganglion/virology
MH  - Viral Load
MH  - *Virus Activation
MH  - *Virus Latency/genetics/physiology
MH  - Virus Replication
PMC - PMC115061
EDAT- 2001/08/03 10:00
MHDA- 2001/09/08 10:01
PMCR- 2001/09/01
CRDT- 2001/08/03 10:00
PHST- 2001/08/03 10:00 [pubmed]
PHST- 2001/09/08 10:01 [medline]
PHST- 2001/08/03 10:00 [entrez]
PHST- 2001/09/01 00:00 [pmc-release]
AID - 0090 [pii]
AID - 10.1128/jvi.75.17.8166-8172.2001 [doi]
PST - ppublish
SO  - J Virol. 2001 Sep;75(17):8166-72. doi: 10.1128/jvi.75.17.8166-8172.2001.