PMID- 19895317
OWN - NLM
STAT- MEDLINE
DCOM- 20100223
LR  - 20091109
IS  - 1460-2202 (Electronic)
IS  - 0271-3683 (Linking)
VI  - 34
IP  - 10
DP  - 2009 Oct
TI  - Expression of herpes virus entry mediator (HVEM) in the cornea and trigeminal 
      ganglia of normal and HSV-1 infected mice.
PG  - 896-904
LID - 10.3109/02713680903184250 [doi]
AB  - PURPOSE: Herpes virus entry mediator (HVEM) plays a critical role in the 
      regulation of inflammation through interaction with its natural ligands LIGHT and 
      lymphotoxin alpha and also serves as one of the entry receptors of herpes simplex 
      virus (HSV). The purpose of this study was to better understand the expression of 
      HVEM in the cornea and trigeminal ganglia (TG), which are important targets of 
      HSV infection. MATERIALS AND METHODS: Immunohistochemistry was used to define 
      HVEM expression in the cornea and TG of normal and HSV-1 infected mice euthanized 
      2 to 5 days or 7 months following corneal inoculation of virus. RESULTS: We found 
      that HVEM is widely expressed in the normal corneal epithelium and endothelium, 
      is weakly and focally expressed in the corneal stroma, and is expressed in a 
      portion of neurons and non-neuronal cells in the TG. Acute HSV-1 keratitis and 
      ganglionitis were associated with increased HVEM expression in the corneal 
      epithelium and stroma and in neurons and non-neuronal cells of TG, and many 
      inflammatory cells in these tissues also expressed HVEM. TG derived from mice 7 
      months after virus inoculation demonstrated latent HSV-1 infection that was 
      associated with increased HVEM expression in neurons and non-neuronal cells 
      relative to uninfected control tissues. Latent TG also contained focal 
      infiltrates of mononuclear inflammatory cells, many of which expressed HVEM. 
      Corneas derived from latently infected mice demonstrated chronic keratitis, with 
      no evidence of virus replication or increased HVEM expression in the corneal 
      epithelium, and inflammatory cells present showed only weak HVEM expression. 
      CONCLUSIONS: HVEM is expressed in the cornea and TG and therefore may serve as an 
      HSV entry receptor in these tissues. Furthermore, these findings raise the 
      possibility that changes in HVEM expression following ocular HSV-1 infection can 
      modulate HSV spread and infection-induced inflammation in the cornea and TG.
FAU - Kovacs, S Krisztian
AU  - Kovacs SK
AD  - Department of Pathology, University of Illinois at Chicago, College of Medicine, 
      Chicago, Illinois 60612, USA.
FAU - Tiwari, Vaibhav
AU  - Tiwari V
FAU - Prandovszky, Emese
AU  - Prandovszky E
FAU - Dosa, Sandor
AU  - Dosa S
FAU - Bacsa, Sarolta
AU  - Bacsa S
FAU - Valyi-Nagy, Klara
AU  - Valyi-Nagy K
FAU - Shukla, Deepak
AU  - Shukla D
FAU - Valyi-Nagy, Tibor
AU  - Valyi-Nagy T
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Curr Eye Res
JT  - Current eye research
JID - 8104312
RN  - 0 (Receptors, Tumor Necrosis Factor, Member 14)
SB  - IM
MH  - Acute Disease
MH  - Animals
MH  - Cell Line
MH  - Cornea/*metabolism/pathology/virology
MH  - Cricetinae
MH  - Female
MH  - *Gene Expression Regulation
MH  - Herpesvirus 1, Human/*physiology
MH  - Humans
MH  - Inflammation/metabolism/virology
MH  - Keratitis, Herpetic/*metabolism/pathology/virology
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Receptors, Tumor Necrosis Factor, Member 14/*biosynthesis/genetics
MH  - Trigeminal Ganglion/*metabolism/pathology/virology
MH  - Virus Internalization
MH  - Virus Latency
MH  - Virus Replication
EDAT- 2009/11/10 06:00
MHDA- 2010/02/24 06:00
CRDT- 2009/11/10 06:00
PHST- 2009/11/10 06:00 [entrez]
PHST- 2009/11/10 06:00 [pubmed]
PHST- 2010/02/24 06:00 [medline]
AID - 10.3109/02713680903184250 [pii]
AID - 10.3109/02713680903184250 [doi]
PST - ppublish
SO  - Curr Eye Res. 2009 Oct;34(10):896-904. doi: 10.3109/02713680903184250.