Herpes simplex virus stromal keratitis

Herpes simplex virus (HSV) stromal keratitis, also known as HSV interstitial keratitis or herpetic stromal keratitis, is an inflammatory condition of the corneal stroma (the middle layer of the cornea) caused by herpes simplex virus infection, most commonly HSV type 1. It represents one of the most serious ocular complications of HSV infection and is a leading infectious cause of corneal blindness in developed countries. The disease primarily affects the eye, specifically the cornea, and results from a combination of direct viral damage and immune-mediated inflammatory responses. Key symptoms include eye pain, redness, tearing, photophobia (sensitivity to light), blurred vision, and progressive corneal opacification (clouding). The stromal inflammation can lead to corneal scarring, neovascularization (abnormal blood vessel growth into the cornea), thinning, and in severe cases, corneal perforation. The condition may present as either necrotizing stromal keratitis, which involves active viral replication and tissue destruction, or immune stromal keratitis, which is primarily driven by the host immune response to viral antigens. Recurrences are common, as HSV establishes latency in the trigeminal ganglion and can reactivate periodically. Treatment typically involves a combination of antiviral medications (such as oral acyclovir or valacyclovir) and topical corticosteroids to control the inflammatory component. The Herpetic Eye Disease Study (HEDS) demonstrated that topical corticosteroids combined with antiviral prophylaxis are effective in managing stromal keratitis. Long-term oral antiviral prophylaxis may be recommended to reduce the frequency of recurrences. In cases where significant corneal scarring has occurred, corneal transplantation (keratoplasty) may be necessary to restore vision, although the risk of recurrence in the graft remains a concern. Some patients with recurrent HSV stromal keratitis have been found to have underlying genetic susceptibility, particularly involving innate immune pathways such as Toll-like receptor 3 (TLR3) signaling deficiencies.

Data sourced from FDA regulatory filings and ClinicalTrials.gov. Updated periodically.

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