PMID- 17898051
OWN - NLM
STAT- MEDLINE
DCOM- 20071218
LR  - 20181113
IS  - 1098-5514 (Electronic)
IS  - 0022-538X (Print)
IS  - 0022-538X (Linking)
VI  - 81
IP  - 23
DP  - 2007 Dec
TI  - A recombinant herpes simplex virus type 1 expressing two additional copies of gK 
      is more pathogenic than wild-type virus in two different strains of mice.
PG  - 12962-72
AB  - The effect of glycoprotein K (gK) overexpression on herpes simplex virus type 1 
      (HSV-1) infection in two different strains of mice was evaluated using a 
      recombinant HSV-1 virus that expresses two additional copies of the gK gene in 
      place of the latency-associated transcript (LAT). This mutant virus (HSV-gK3) 
      expressed higher levels of gK than either the wild-type McKrae virus or the 
      parental dLAT2903 virus both in vitro (in cultured cells) and in vivo (in 
      infected mouse corneas and trigeminal ganglia [TG] of BALB/c and C57BL/6 mice). 
      gK transcripts were detected in the TG of both HSV-gK3-infected mouse strains on 
      day 30 postinfection (p.i.), while gB transcripts were detected only in the TG of 
      the HSV-gK3-infected C57BL/6 mice, a finding that suggests that increased gK 
      levels promote chronic infection. C57BL/6 mice infected with HSV-gK3 also 
      contained free virus in their TG on day 30 p.i. Both HSV-gK3-infected mouse 
      strains had significantly higher corneal scarring (CS) than did McKrae-infected 
      mice. T-cell depletion studies in C57BL/6 mice suggested that this CS enhancement 
      in the HSV-gK3-infected mice was mediated by a CD8+ T-cell response. Taken 
      together, these results strongly suggest that increased gK levels promote eye 
      disease and chronic infection in infected mice.
FAU - Mott, Kevin R
AU  - Mott KR
AD  - Center for Neurobiology and Vaccine Development, Ophthalmology Research, 
      Department of Surgery, Cedars-Sinai Burns & Allen Research Institute, CSMC-D2024, 
      8700 Beverly Blvd., Los Angeles, California 90048, USA.
FAU - Perng, Guey-Chuen
AU  - Perng GC
FAU - Osorio, Yanira
AU  - Osorio Y
FAU - Kousoulas, Konstantin G
AU  - Kousoulas KG
FAU - Ghiasi, Homayon
AU  - Ghiasi H
LA  - eng
GR  - R01 EY013615/EY/NEI NIH HHS/United States
GR  - EY13615/EY/NEI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20070926
PL  - United States
TA  - J Virol
JT  - Journal of virology
JID - 0113724
RN  - 0 (MicroRNAs)
RN  - 0 (UL53 protein, Human herpesvirus 1)
RN  - 0 (Viral Proteins)
RN  - 0 (Virulence Factors)
RN  - 0 (latency associated transcript, herpes simplex virus-1)
SB  - IM
MH  - Animals
MH  - CD8-Positive T-Lymphocytes/immunology
MH  - Cells, Cultured
MH  - Cornea/pathology
MH  - Gene Deletion
MH  - Gene Dosage
MH  - Herpesviridae Infections
MH  - Herpesvirus 1, Human/genetics/*pathogenicity
MH  - Lymphocyte Depletion
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Mice, Inbred C57BL
MH  - MicroRNAs
MH  - Trigeminal Ganglion/virology
MH  - Viral Proteins/genetics/*physiology
MH  - Virulence Factors/genetics/*physiology
PMC - PMC2169076
EDAT- 2007/09/28 09:00
MHDA- 2007/12/19 09:00
PMCR- 2008/04/01
CRDT- 2007/09/28 09:00
PHST- 2007/09/28 09:00 [pubmed]
PHST- 2007/12/19 09:00 [medline]
PHST- 2007/09/28 09:00 [entrez]
PHST- 2008/04/01 00:00 [pmc-release]
AID - JVI.01442-07 [pii]
AID - 1442-07 [pii]
AID - 10.1128/JVI.01442-07 [doi]
PST - ppublish
SO  - J Virol. 2007 Dec;81(23):12962-72. doi: 10.1128/JVI.01442-07. Epub 2007 Sep 26.