Abstract

Varicella zoster virus (VZV) is a ubiquitous neurotropic alphaherpesvirus that typically causes childhood varicella (chickenpox) on primary infection and zoster (shingles) after reactivation. During latency most of the ~70 virus genes are transcriptionally silent; however, analysis of latent VZV gene transcription in its natural setting requires analysis of human ganglia removed at autopsy. Recognizing the problems associated with such samples, we have observed that as the post-mortem time interval increases, so do the number of VZV genes transcribed. Based on our data and recent similar findings concerning reactivation of HSV-1, we propose an interesting testable model to describe epigenetic control of neurotropic alphaherpesvirus gene transcription during latency and early reactivation.

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