Purpose: A retrospective cross-section study to analyze the prevalence of herpes simplex virus–induced keratitis (HSK) among 3,000 patients attending a corneal clinic in South India between 1995 and 1997, and to evaluate laboratory techniques for detecting HSK. Although carefully collected, accuracy cannot be guaranteed. Two patients with RA presented with painful red right eyes. Several commercially available topical and oral antiviral drugs for HSK are currently available. To determine the effect on recurrences of herpetic keratitis, animals infected with McKrae strain herpes simplex virus type 1 that survived to day 32 after infection were randomized to treatment with latanoprost 0.005% or balanced saline solution and evaluated for the presence of corneal lesions from postinfection day 32 to day 47. Unoprostone-treated and saline-treated eyes showed no significant difference in the frequency of recurrent lesions. Visual morbidity results from recurrent keratitis, which leads to corneal scarring, thinning and neovascularisation.
Further, local cDC depletion resulted in decreased corneal nerve infection, and subsequently decreased and delayed systemic viral transmission in the trigeminal ganglion and draining lymph node, resulting in decreased mortality of mice. The pathogenesis and severity of HSK is largely determined by an interaction between viral genes encoded by the strain of HSV-1 and the make up of the host’s immune system. Herpetic stromal disease is due to the immune response to virus within the cornea and the ability of the strain to cause corneal stromal disease is correlated with its ability to induce corneal vascularisation. The condition resolved after treatment with oral antiviral medication. Dendritic cell autophagy did not alter immune control of the virus or neurological disease but specifically augmented CD4+ T cell activation and pathological corneal inflammation. Thrombospondin 1 and 2, matricellular proteins, involved in wound healing are potent anti-angiogenic factors and appear to be one of the key players. Elucidating their roles in corneal scarring and vascularisation may lead to improved therapies for HSK.