Varicella zoster virus infection: clinical features, molecular pathogenesis of disease, and latency.

Varicella zoster virus (VZV) is an exclusively human neurotropic alphaherpesvirus. Primary infection causes varicella (chickenpox), after which virus becomes latent in cranial nerve ganglia, dorsal root ganglia, and autonomic ganglia along the entire neuraxis. Years later, in association with a decline in cell-mediated immunity in elderly and immunocompromised individuals, VZV reactivates and causes a wide range of neurologic disease. This article discusses the clinical manifestations, treatment, and prevention of VZV infection and reactivation; pathogenesis of VZV infection; and current research focusing on VZV latency, reactivation, and animal models.

Intrathecal antibody production against viruses of the herpesvirus family in acute retinal necrosis syndrome.

Viruses of the herpesvirus family cause acute retinal necrosis syndrome, a devastating necrotic retinitis in immunocompetent individuals. Direct proof of the viral origin of this disease may be obtained by demonstration of the virus, viral antigens, or viral DNA in biopsy specimens of retinas. In search of alternative diagnostic methods, we analyzed cerebrospinal fluid and serum with enzyme-linked immunosorbent assays for virus-specific antibody activity. Intrathecally produced viral antibodies were found in three consecutive patients with acute retinal necrosis syndrome: herpes simplex type 2 in a 30-year-old woman with a history of suspected neonatal herpes encephalitis, herpes simplex type 1 in a 35-year-old man, and varicella-zoster virus activity in a 62-year-old woman. None of the patients had clinical signs indicating an acute disorder in the central nervous system. This serologic approach seems to be of value for the diagnosis of an associated intracerebral viral infection in cases of acute retinal necrosis syndrome.

[Cerebrospinal fluid analysis in Kirisawa-Urayama type uveitis].

PURPOSE: We investigated whether viral encephalitis could occur in patients with Kirisawa-Urayama type uveitis by analysing the cerebrospinal fluid (CSF). METHODS: CSF samples were aspirated from nine patients with Kirisawa-Urayama type uveitis and assayed for local antibody production and the presence of herpesvirus DNA. RESULTS: Seven cases had mild CSF pleocytosis. In six of seven cases who underwent CSF antibody analysis, we found intrathecal antibody production against herpes simplex virus or varicella-zoster virus which were the causative viruses diagnosed from intraocular fluid in each patients. Polymerase chain reaction (PCR) assay was used to search for virus DNA in the CSF of six patients, but all were negative. CONCLUSIONS: The results of this study suggest that Kirisawa-Urayama type uveitis is often accompanied with optic nerve involvement and intrathecal antibody production against causative viruses, but we could not find any viral encephalitis.