Ocular inflammation with varicella-zoster virus and immune privilege

Mice with experimental acute retinal necrosis (ARN) induced by herpes simplex virus fail to acquire virus-specific delayed hypersensitivity (DH), even though they produce antiviral antibodies. We investigated whether there was a similar correlation for patients with varicella zoster virus(VZV)-induced ARN or patients with anterior uveitis caused by VZV. Patients with acute, VZV-induced ARN, with anterior uveitis with dermatitis(herpes zoster ophthalmicus, ZO-AU), or with anterior uveitis without dermatitis(zoster sine herpete, ZSH-AU) were skin-tested with VZV to evaluate DH. All patients with VZV-induced skin disease alone(control group) displayed intense DH when tested with VZV antigen. In contrast, subsets of patients with ARN or ZO-AU displayed absent VZV-specific DH. Patients with the most severe ARN or ZO-AU had the lowest DH responses to VZV antigens. Serum anti-VZV antibody titers were higher in ARN patients than in normal subjects, and anti-viral titer correlated inversely with intensity of anti-VZV DH responses. VZV-specific DH responses were restored in patients who recovered from ARN or from anterior uveitis caused by VZV. Patients with ZSH-AU also failed to display VZV-specific DH. Absence of DH reactivity to VZV antigens appears to be a concomitant feature of VZV-uveitis of high intensity.