Detection of varicella zoster virus DNA and viral antigen in human eyes after herpes zoster ophthalmicus

Abstract

Objective: The purpose of the study was to identify varicella zoster virus (VZV) DNA and viral antigen in human eyes at various intervals after clinical onset of herpes zoster ophthalmicus (HZO).

Design: A retrospective case series.

Participants: There were 9 eyes and 4 corneal buttons surgically obtained from 13 patients with HZO at the University Eye Hospital of Erlangen-Nürnberg between 1984 and 1994. Specimens were examined at different timepoints after clinical onset of HZO (range, 1 day-19 years; median, 36 months).

Methods: Histopathologic evaluation was performed on formalin-fixed and paraffin-embedded tissue by routine histology, immunohistochemistry (5-B-7 murine monoclonal antibody to VZV; peroxidase-antiperoxidase method), and DNA-in situ hybridization (35S deoxyadenosine triphosphate-labeled HindIII fragments [A and C] of VZV).

Results: Typical histopathologic changes associated with HZO were identified: vascularization of the corneal stroma (11 of 13), granulomatous reaction to Descemet's membrane (8 of 13), fusiform-shaped ciliary scarring (5 of 9), optic neuritis (4 of 9), and perineuritis (8 of 9) and perivasculitis (8 of 9) of the long posterior ciliary nerves and arteries. VZV antigen was detected in two patients with acute infection 1 and 7 days after onset of HZO, respectively. VZV-DNA was identified in seven patients up to 10 years after onset of HZO in corneal epithelial cells (2 of 13), corneal stroma (5 of 13), inflammatory infiltrate of the anterior chamber (1 of 9), episclera (2 of 9), posterior ciliary nerves (1 of 9) and arteries (5 of 9), optic nerve (5 of 9), and adjacent leptomeninges (2 of 9).

Conclusion: Persistence of viral genomes, most likely accompanied by gene expression or slow viral replication, appears to be responsible for the often smoldering panophthalmitis and the chronic recurrent keratouveitis in patients with HZO. Localization of viral DNA in vascular structures suggests a role for vasculitis in the pathogenesis of some ocular findings associated with HZO.