Abstract
Viral infections of the ocular surface (OS) may cause chronic, and/or recurrent inflammation that disrupt OS homeostasis, impact quality of life, and potentially impair vision through loss of corneal transparency and/or regularity. In this presentation, we'll review basic and clinical findings underlying OS inflammation in the context of the 3 most common viral pathogens affecting the OS, i.e. Adenovirus, Herpes Simplex virus type 1 and Varicella Zoster Virus.During its acute replicative phase, adenoviral keratoconjunctivitis may trigger severe acute conjunctival inflammation, leading to transmucosal exudation and fibrinous pseudo‐membrane formation. If left untreated, the latter induce conjunctival fibrosis with extensive loss of goblet cells. In a second phase of the disease, antigen‐driven immune‐mediated mechanisms may cause chronic corneal subepithelial infiltration.In the context of HSV and VZV keratitis, OS inflammation is caused by a combination of specific immune response to viral replication, causing stromal infiltration, and neovascularisation and ii) non‐specific inflammatory processes caused by corneal innervation alterations that impact tear secretion and osmolarity. While clinical disease is most often unilateral, unaffected side may display subclinical alterations, including decrease in corneal sensitivity and corneal nerve density, and decrease in endothelial cell density.Management of viral ocular surface inflammation involves a combination of strategies aiming at controlling viral replication, decrease associated inflammatory/immune response and restore OS homeostasia.
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