AIMS: To investigate the role of herpes virus entry mediator (HVEM) in viral entry and inflammatory cytokine production in response to herpes simplex virus (HSV) type 1 challenge in human corneal epithelial cells. METHODS: HVEM expression in human corneal epithelial cells was determined by immunofluorescence and flow cytometry. The HSV-1 virus expressing β-galactosidase was used to challenge corneal epithelial cells and viral entry assays were performed to ascertain HSV-1 entry into cells. Levels of cytokines TNF-α, IL-6, IFN-x03B3;, IL-12, and IL-18 and chemokines MIP-1α, MIP-1β and MIP-2 were detected in corneal epithelial cells treated with control or HVEM siRNA in response to HSV-1 challenge. RESULTS: Human corneal epithelial cells were positive for HVEM expression and showed high susceptibility to HSV-1 entry. Silencing of HVEM did not alter viral entry dramatically. However, levels of the cytokine IFN-x03B3; and chemokines MIP-1α and MIP-1β were measured to be higher in HVEM siRNA-treated cells than control after HSV-1 challenge. CONCLUSIONS: HVEM in human corneal epithelial cells may act to dampen the production of some cytokines and chemokines and thus it may modulate the innate immune response against HSV-1. This may provide a novel mechanism for the pathogenesis of HSV-1 infection in the cornea.
AIMS: To investigate the role of herpes virus entry mediator (HVEM) in viral entry and inflammatory cytokine production in response to herpes simplex virus (HSV) type 1 challenge in human corneal epithelial cells. METHODS:HVEM expression in human corneal epithelial cells was determined by immunofluorescence and flow cytometry. The HSV-1 virus expressing β-galactosidase was used to challenge corneal epithelial cells and viral entry assays were performed to ascertain HSV-1 entry into cells. Levels of cytokines TNF-α, IL-6, IFN-x03B3;, IL-12, and IL-18 and chemokines MIP-1α, MIP-1β and MIP-2 were detected in corneal epithelial cells treated with control or HVEM siRNA in response to HSV-1 challenge. RESULTS:Human corneal epithelial cells were positive for HVEM expression and showed high susceptibility to HSV-1 entry. Silencing of HVEM did not alter viral entry dramatically. However, levels of the cytokine IFN-x03B3; and chemokines MIP-1α and MIP-1β were measured to be higher in HVEM siRNA-treated cells than control after HSV-1 challenge. CONCLUSIONS:HVEM in human corneal epithelial cells may act to dampen the production of some cytokines and chemokines and thus it may modulate the innate immune response against HSV-1. This may provide a novel mechanism for the pathogenesis of HSV-1 infection in the cornea.