Expression of Herpes Virus Entry Mediator (HVEM) in the Cornea and Trigeminal Ganglia of Normal and HSV-1 Infected Mice

Autor:	Tibor Valyi-Nagy, Klara Valyi-Nagy, S. Krisztian Kovacs, Sarolta Bacsa, Deepak Shukla, Emese Prandovszky, Vaibhav Tiwari, Sandor Dosa
Rok vydání:	2009
Předmět:	Lymphotoxin alpha Pathology medicine.medical_specialty viruses Herpesvirus 1 Human Biology Virus Replication medicine.disease_cause Cell Line Keratitis Cornea Mice Cellular and Molecular Neuroscience Stroma Cricetinae Virus latency medicine Animals Humans Corneal epithelium Inflammation Mice Inbred BALB C Virus Internalization medicine.disease eye diseases Sensory Systems Virus Latency Ophthalmology medicine.anatomical_structure Herpes simplex virus Gene Expression Regulation Trigeminal Ganglion Acute Disease Immunology Keratitis Herpetic Female Tumor necrosis factor alpha sense organs Receptors Tumor Necrosis Factor Member 14
Zdroj:	Current Eye Research. 34:896-904
ISSN:	1460-2202 0271-3683
DOI:	10.3109/02713680903184250
Popis:	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.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.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.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.
Databáze:	OpenAIRE
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