No Evidence of Varicella-Zoster Virus Infection in Temporal Artery Biopsies of Anterior Ischemic Optic Neuropathy Patients With and Without Giant Cell Arteritis.

BACKGROUND: To test the hypothesis that varicella-zoster virus (VZV) infection contributes to temporal arteritis pathogenesis, comprehensive in situ analysis was performed on temporal artery biopsies of 38 anterior ischemic optic neuropathy (AION) patients, including 14 (37%) with giant cell arteritis. METHODS: Biopsies were completely sectioned, and, on average, 146 serial sections per patient were stained for VZV glycoprotein E. RESULTS: Four of 38 AION patients showed VZV glycoprotein E staining, but VZV infection was not confirmed by staining for VZV IE63 protein and VZV-specific polymerase chain reaction on adjacent sections. CONCLUSIONS: This study refutes the premise that VZV is casually related to AION with and without giant cell arteritis.

Varicella zoster virus ischemic optic neuropathy and subclinical temporal artery involvement.

OBJECTIVE: To demonstrate varicella zoster virus (VZV) infection in an asymptomatic extracranial (temporal) artery in a patient with ischemic optic neuropathy produced by VZV vasculopathy in whom the pathological changes were mistakenly identified as giant cell arteritis. DESIGN: Case report. SETTING: Teaching hospital, pathology and virology laboratory. PATIENT: An 80-year-old man with left ophthalmic distribution zoster who developed left ischemic optic neuropathy. INTERVENTION: An ipsilateral temporal artery biopsy revealed inflammation that was mistakenly identified as giant cell arteritis. The patient was initially treated with steroids but his condition did not improve. When the diagnosis of VZV vasculopathy was confirmed virologically and the patient was treated with intravenous acyclovir, his vision improved. RESULTS: Pathological and virological studies provided proof of VZV vasculopathy in the asymptomatic temporal artery. Varicella zoster virus antigen was abundant in arterial adventitia and scattered throughout the media. With intravenous antiviral therapy, the patient's vision improved. CONCLUSION: Although in previously studied patients who died of chronic VZV vasculopathy after 10 to 12 months, VZV antigen was present exclusively in the intima, collective analyses of chronic cases and the asymptomatic VZV-infected temporal artery suggest that virus enters arteries through the adventitia and spreads transmurally to the intima.

[Ocular manifestations during hepatitis C infection]. / Objawy oczne u chorych zakazonych wirusem C zapalenia watroby (HCV).

Hepatitis C wirus is one of the major blood-born pathogens of huge epidemic value. Due to its easy transmission, lack of routinely pursued tests and long non-symptomatic period makes it crucial to be alert for all co-morbidites suggesting HCV infection. Consequently to reduce its farther transmission large knowledge of HCV should be spread as there is still no effective means of prophylaxis and its therapy is much costly. This article describes ophthalmic symptoms of hepatitis C virus infection such a mere keratoconiunctivitis sicca to ischemic retinopathy, macular edema and ischemic neuropathy.