PMID- 10683323
OWN - NLM
STAT- MEDLINE
DCOM- 20000329
LR  - 20201208
IS  - 0042-6822 (Print)
IS  - 0042-6822 (Linking)
VI  - 268
IP  - 1
DP  - 2000 Mar 1
TI  - Establishment of latent herpes simplex virus type 1 infection in resistant, 
      sensitive, and immunodeficient mouse strains.
PG  - 17-28
AB  - Productive infection with herpes simplex virus (HSV) type 1 is limited by both 
      innate and adaptive immune mechanisms. The purpose of the current study was to 
      determine whether these mechanisms also play a role in the establishment of 
      latent HSV infection. First we examined the trigeminal ganglia (TG) of severe 
      combined immunodeficiency (SCID), interferon-gamma knockout (GKO), and beige (a 
      strain deficient in natural killer cell activity) mice following ocular 
      inoculation with HSV. Although infection of SCID mice was invariably lethal, we 
      consistently found latently infected neurons in the TG of these animals at 2-4 
      days postinoculation. HSV infection of GKO and beige mice, while not lethal, was 
      characterized by a greater number of productively infected TG neurons and/or a 
      delay in the time to peak productive infection compared to C57BL/6 controls. 
      However, as assayed by both in situ hybridization for LAT expression and 
      quantitative PCR (Q-PCR) for viral DNA, we found that HSV established a latent 
      infection in GKO and beige mice as efficiently as in C57BL/6 controls. We 
      subsequently examined the TG of "HSV-sensitive" strains of mice (Swiss-Webster, 
      CBA, and BALB/c) following ocular infection with HSV. At the peak of acute 
      ganglionic infection the number of productively infected TG neurons in each of 
      these mouse strains was about sevenfold greater than in the "HSV-resistant" 
      strain C57BL/6, consistent with previously reported differences in susceptibility 
      to lethal challenge with HSV. However, as assayed by both in situ hybridization 
      for LAT and Q-PCR for viral DNA, we found that HSV established a latent infection 
      in Swiss-Webster, CBA, and BALB/c mice as efficiently as in C57BL/6 controls. We 
      conclude that HSV efficiently establishes latent infection in the TG of mice in 
      the absence of innate and adaptive immune mechanisms that are essential for 
      limiting productive viral infection.
CI  - Copyright 2000 Academic Press.
FAU - Ellison, A R
AU  - Ellison AR
AD  - Francis I. Proctor Foundation, Department of Ophthalmology, University of 
      California at San Francisco Medical Center, 95 Kirkham Street, San Francisco, 
      California, 94143, USA.
FAU - Yang, L
AU  - Yang L
FAU - Voytek, C
AU  - Voytek C
FAU - Margolis, T P
AU  - Margolis TP
LA  - eng
GR  - NIH02162/PHS HHS/United States
GR  - NIH10008/PHS HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Virology
JT  - Virology
JID - 0110674
RN  - 0 (DNA, Viral)
RN  - 0 (Intracellular Signaling Peptides and Proteins)
RN  - 0 (Lyst protein, mouse)
RN  - 0 (Proteins)
RN  - 0 (RNA, Viral)
RN  - 0 (Vesicular Transport Proteins)
RN  - 82115-62-6 (Interferon-gamma)
SB  - IM
MH  - Animals
MH  - B-Lymphocytes/immunology
MH  - DNA, Viral/analysis
MH  - Disease Susceptibility
MH  - Herpes Simplex/*immunology/virology
MH  - Herpesvirus 1, Human/*immunology/*physiology
MH  - Immunity, Innate
MH  - Interferon-gamma/genetics/immunology
MH  - Intracellular Signaling Peptides and Proteins
MH  - Killer Cells, Natural/immunology
MH  - Mice
MH  - Mice, Inbred Strains
MH  - Mice, Knockout
MH  - Mice, SCID
MH  - Neurons/virology
MH  - Proteins/genetics
MH  - RNA, Viral/analysis
MH  - T-Lymphocytes/immunology
MH  - Trigeminal Ganglion/*virology
MH  - Vesicular Transport Proteins
MH  - Virus Latency
EDAT- 2000/02/23 09:00
MHDA- 2000/04/01 09:00
CRDT- 2000/02/23 09:00
PHST- 2000/02/23 09:00 [pubmed]
PHST- 2000/04/01 09:00 [medline]
PHST- 2000/02/23 09:00 [entrez]
AID - S0042-6822(99)90158-7 [pii]
AID - 10.1006/viro.1999.0158 [doi]
PST - ppublish
SO  - Virology. 2000 Mar 1;268(1):17-28. doi: 10.1006/viro.1999.0158.