PMID- 11773630
OWN - NLM
STAT- MEDLINE
DCOM- 20020429
LR  - 20181113
IS  - 0027-8424 (Print)
IS  - 1091-6490 (Electronic)
IS  - 0027-8424 (Linking)
VI  - 99
IP  - 2
DP  - 2002 Jan 22
TI  - Spontaneous molecular reactivation of herpes simplex virus type 1 latency in 
      mice.
PG  - 978-83
AB  - Infection of the mouse trigeminal ganglia (TG) is the most commonly used model 
      for the study of herpes simplex virus type 1 (HSV-1) latency. Its popularity is 
      caused, at least in part, by the perception that latent infection can be studied 
      in this system in the absence of spontaneous viral reactivation. However, this 
      perception has never been rigorously tested. To carefully study this issue, the 
      eyes of Swiss-Webster mice were inoculated with HSV-1 (KOS), and 37-47 days later 
      the TG were dissected, serial-sectioned, and probed for HSV-1 ICP4, thymidine 
      kinase, glycoprotein C, and latency-associated transcript RNA by in situ 
      hybridization. Serial sections of additional latently infected TG were probed 
      with HSV-1-specific polyclonal antisera. Analysis of thousands of probed sections 
      revealed abundant expression of viral transcripts, viral protein, and viral DNA 
      replication in about 1 neuron per 10 TG tested. These same neurons were 
      surrounded by a focal white cell infiltrate, indicating the presence of an 
      antigenic stimulus. We conclude that productive cycle viral genes are abundantly 
      expressed in rare neurons of latently infected murine TG and that these events 
      are promptly recognized by an active local immune response. In the absence of 
      detectable infectious virus in these ganglia, we propose the term "spontaneous 
      molecular reactivation" to describe this ongoing process.
FAU - Feldman, Lawrence T
AU  - Feldman LT
AD  - Department of Microbiology and Immunology, University of California Medical 
      Center, Los Angeles, CA 90024, USA.
FAU - Ellison, Aaron R
AU  - Ellison AR
FAU - Voytek, Cynthia C
AU  - Voytek CC
FAU - Yang, Li
AU  - Yang L
FAU - Krause, Philip
AU  - Krause P
FAU - Margolis, Todd P
AU  - Margolis TP
LA  - eng
GR  - EY10008/EY/NEI NIH HHS/United States
GR  - AI45679/AI/NIAID NIH HHS/United States
GR  - R01 EY010008/EY/NEI NIH HHS/United States
GR  - EY02162/EY/NEI NIH HHS/United States
GR  - R01 AI045679/AI/NIAID NIH HHS/United States
GR  - P30 EY002162/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.
DEP - 20020102
PL  - United States
TA  - Proc Natl Acad Sci U S A
JT  - Proceedings of the National Academy of Sciences of the United States of America
JID - 7505876
RN  - 0 (Antigens, Viral)
RN  - 0 (DNA, Viral)
RN  - 0 (Immediate-Early Proteins)
RN  - 0 (RNA, Viral)
RN  - 0 (Viral Envelope Proteins)
RN  - 0 (glycoprotein gC, herpes simplex virus type 1)
RN  - 0 (herpes simplex virus, type 1 protein ICP4)
RN  - EC 2.7.1.21 (Thymidine Kinase)
SB  - IM
MH  - Animals
MH  - Antigens, Viral/genetics
MH  - DNA, Viral/genetics/metabolism
MH  - Female
MH  - Gene Expression
MH  - Genes, Viral
MH  - Herpesvirus 1, Human/*genetics/immunology/*pathogenicity
MH  - Immediate-Early Proteins/genetics
MH  - In Situ Hybridization
MH  - Keratitis, Herpetic/etiology/pathology/virology
MH  - Mice
MH  - RNA, Viral/genetics/metabolism
MH  - Thymidine Kinase/genetics
MH  - Time Factors
MH  - Trigeminal Ganglion/pathology/virology
MH  - Viral Envelope Proteins/genetics
PMC - PMC117416
EDAT- 2002/01/05 10:00
MHDA- 2002/05/01 10:01
PMCR- 2002/07/22
CRDT- 2002/01/05 10:00
PHST- 2002/01/05 10:00 [pubmed]
PHST- 2002/05/01 10:01 [medline]
PHST- 2002/01/05 10:00 [entrez]
PHST- 2002/07/22 00:00 [pmc-release]
AID - 022301899 [pii]
AID - 3018 [pii]
AID - 10.1073/pnas.022301899 [doi]
PST - ppublish
SO  - Proc Natl Acad Sci U S A. 2002 Jan 22;99(2):978-83. doi: 10.1073/pnas.022301899. 
      Epub 2002 Jan 2.