Like HSV-1, VZV is a double-stranded DNA virus which, in humans, has a propensity to reside in a latent, noninfective state in sensory neural ganglia; unlike HSV-1, however, VZV cannot be cultured from human ganglia cells. Unlike herpes simplex reactivation, VZV reactivation causes serum antibody levels to rise during virus reactivation. Neurologic damage begins before the characteristic rash appears. Studies using PCR analysis have found the genome in blood vessels and in other types of tissue. The mechanisms causing reactivation of VZV to an active infective state have not been identified (23).
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