PMID- 17686862
OWN - NLM
STAT- MEDLINE
DCOM- 20080108
LR  - 20220311
IS  - 0022-538X (Print)
IS  - 1098-5514 (Electronic)
IS  - 0022-538X (Linking)
VI  - 81
IP  - 20
DP  - 2007 Oct
TI  - Spontaneous reactivation of herpes simplex virus type 1 in latently infected 
      murine sensory ganglia.
PG  - 11069-74
AB  - Careful studies of mouse trigeminal ganglia (TG) latently infected with herpes 
      simplex virus type 1 (HSV-1) indicate the presence of productive cycle viral gene 
      products and persistent immune response, suggesting ongoing spontaneous viral 
      reactivation in these tissues. In the present study we set out to determine 
      whether infectious virus is present in murine TG latently infected with HSV-1 
      (KOS). At 37 days after ocular inoculation we found a small amount of infectious 
      virus in ca. 6% of latently infected murine TG. Furthermore, the amount of 
      infectious virus that we detected (PFU per viral antigen-positive neuron) was 
      similar to that detected in acutely infected ganglia. We conclude that 
      spontaneous reactivation of infectious HSV-1 occurs in the mouse TG and is likely 
      the principle cause of viral protein expression in these tissues. We next 
      examined the role of latency-associated transcript (LAT) in spontaneous 
      ganglionic reactivation by examining ganglia latently infected with KOS dlLAT1.8, 
      a LAT deletion virus. Through the use of immunocytochemistry we found that KOS 
      dlLAT1.8 had a rate of spontaneous ganglionic reactivation very similar to that 
      of HSV-1 (KOS). Studying spontaneous ganglionic reactivation of HSV in the mouse 
      TG allows a direct study of viral reactivation from latently infected neurons 
      without the potential confounders and complicating downstream events that 
      accompany the study of viral reactivation by explantation or peripheral viral 
      shedding. Since most cases of human viral shedding and reactivation are not 
      associated with a known trigger, spontaneous ganglionic reactivation of HSV-1 may 
      be a better model of human disease than existing models.
FAU - Margolis, Todd P
AU  - Margolis TP
AD  - Francis I. Proctor Foundation, UCSF, Medical Sciences Building S-310, 513 
      Parnassus Ave., San Francisco, CA 94143-0412, USA. todd.margolis@ucsf.edu
FAU - Elfman, Fred L
AU  - Elfman FL
FAU - Leib, David
AU  - Leib D
FAU - Pakpour, Nazzy
AU  - Pakpour N
FAU - Apakupakul, Kathleen
AU  - Apakupakul K
FAU - Imai, Yumi
AU  - Imai Y
FAU - Voytek, Cindy
AU  - Voytek C
LA  - eng
GR  - EY10008/EY/NEI NIH HHS/United States
GR  - EY09083/EY/NEI NIH HHS/United States
GR  - R01 EY009083/EY/NEI NIH HHS/United States
GR  - R01 EY010008/EY/NEI NIH HHS/United States
GR  - EY02162/EY/NEI NIH HHS/United States
GR  - P30 EY002162/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 - 20070808
PL  - United States
TA  - J Virol
JT  - Journal of virology
JID - 0113724
RN  - 0 (Viral Proteins)
SB  - IM
MH  - Animals
MH  - Ganglia, Sensory/*virology
MH  - Herpesvirus 1, Human/*physiology
MH  - Mice
MH  - Viral Load
MH  - Viral Proteins/genetics
MH  - *Virus Activation
MH  - *Virus Latency
PMC - PMC2045564
EDAT- 2007/08/10 09:00
MHDA- 2008/01/09 09:00
PMCR- 2008/02/01
CRDT- 2007/08/10 09:00
PHST- 2007/08/10 09:00 [pubmed]
PHST- 2008/01/09 09:00 [medline]
PHST- 2007/08/10 09:00 [entrez]
PHST- 2008/02/01 00:00 [pmc-release]
AID - JVI.00243-07 [pii]
AID - 0243-07 [pii]
AID - 10.1128/JVI.00243-07 [doi]
PST - ppublish
SO  - J Virol. 2007 Oct;81(20):11069-74. doi: 10.1128/JVI.00243-07. Epub 2007 Aug 8.