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Demonstration of herpes simplex virus from lens aspirate in healed acute retinal necrosis syndrome
  1. Medical and Vision Research Foundation, 18 College Road, Madras - 600 006, India
  1. Dr Jyotirmay Biswas.

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Editor,—The herpes group of viruses, mainly the varicella zoster virus (HZV), and more rarely, the herpes simplex (HSV) types 1 and 2, and cytomegalovirus (CMV),1 have been demonstrated in aqueous humour,2 vitreous,3or retinal biopsy4 specimens in the active phase of acute retinal necrosis (ARN), by isolation, immunological methods, electron microscopy, and polymerase chain reaction. However, several reports indicate the inability to demonstrate the virus from intraocular specimens in the healed stage of the disease.45

We report a case of ARN in which HSV 1 was isolated from intraocular fluid containing lens aspirate, 3½ months after complete regression of the disease. We believe that this is the first such original finding to be reported.


A 23-year-old man presented with a history of headache, sudden blurring of vision, and mild pain in the left eye for 3 weeks. Six years earlier the patient had lost his vision in the right eye following an acute attack of inflammation, the details of which were not known.

His vision was no light perception in the right eye and 6/36 in the left eye. The right eye had band-shaped keratopathy, organised exudates in the anterior chamber, and complicated cataract. The left eye showed multiple large keratic precipitates, aqueous flare 2+, aqueous cells 2+. There was no view of the fundus in the right eye. The left fundus showed typical confluent areas of retinal necrosis in the mid periphery with vitreous haze, suggestive of ARN.

The patient was treated with intravenous aciclovir 1500 mg/m2 of body surface area/day in three divided doses, oral prednisolone, 40 mg per day, topical betamethasone hourly, and atropine twice daily, for 1 week. His visual acuity improved to 6/18 in the left eye with regression of inflammation. He was then treated with oral aciclovir 400 mg, five times daily for 4 weeks. But subsequently the patient developed dense vitreous membranes obscuring the fundus details and a pars plana vitrectomy was carried out 10 days later. Vitreous aspirate on immunofluorescence (IF), using a panel of antisera of HSV (Dako A/S, Denmark), VZV (polyclonal human serum), and CMV (Dako A/S, Denmark) showed the HSV viral antigen. Vitreous aspirate also revealed both anti-HSV IgM and IgG at >1:40 dilutions by enzyme linked immunosorbent test assay (ELISA). An ELISA test for HZV and CMV showed no antibody. A week later, the retina detached and was reattached by revitrectomy with scleral buckling. On follow up after 1 month there was complete regression of retinitis with scarring and no evidence of inflammation in the anterior segment or vitreous cavity. However, vision deteriorated due to progressive nuclear sclerosis. An extracapsular cataract extraction with intraocular lens implantation was performed 3½ months later. The lens aspirate was inoculated into vero cell line. It showed the growth with the characteristic cytopathic effect of HSV. The isolated virus was identified as HSV by IF (Fig 1) which was further confirmed by a neutralisation test as HSV type 1 using HSV 1 and HSV 2 antisera. CMV and VZV were not isolated. The patient had no evidence of active retinitis at 2 months’ follow up after cataract extraction.

Figure 1

Microphotograph showing HSV antigen in vero cells inoculated with lens aspirate detected by immunofluorescence (magnification × 112).


Thompson et al have reported three cases of ARN due to possible reactivation of HSV type 2.6 Recurrence in ARN, though rare, has been reported in the same eye even after 6 years.7 Our case indicates that the virus causing ARN can remain viable in the eye long after clinical regression, and can probably play a potential role in recurrence due to reactivation.


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