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Hui Guo, Xinyi Wu, Kunpeng Pang; HVEM in corneal epithelial cells modulates the innate immune response against HSV type 1. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):1854.
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© ARVO (1962-2015); The Authors (2016-present)
Herpes simplex virus (HSV) type 1 infection of the eye is one of the leading infectious causes of vision impairment. Recent studies provide evidence for HSV-1 latency in corneal cells, thus HSV-1 may utilize unique mechanism to <br /> escape from innate immunity and to be latent at the cornea. Infection of cells with HSV-1 is initiated by <br /> specific interactions of viral envelope glycoprotein D with host cell surface receptor herpes virus entry mediator (HVEM). The objective of the present study was to investigate the role of HVEM in the viral entry and innate immune response to HSV-1 challenge in human corneal epithelial cells.
HVEM expression in human corneal epithelial cells was detected by immunofluorescence and flow cytometry. Viral entry assays were performed to detect HSV-1 entry into human corneal epithelial cells.<br /> Then real time PCR and Enzyme Linked Immunosorbent Assay was performed to detect the levels of cytokines and chemokines in corneal epithelial cells treated with control or HVEM siRNA in response to HSV-1 challenge.
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-gamma and chemokines MIP-1 alpha, MIP-1 beta were measured to be higher in HVEM siRNA-treated cells than control siRNA-treated cells after HSV-1 challenge.
Our results suggest that HVEM in human corneal epithelial cells may act to dampen these responses and may modulate the innate immune response against HSV-1,apart from allowing the virus to enter cells. This may provide a novel mechanism<br /> for immune evasion and latency by HSV-1 in corneal epithelial cells.
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