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33 - HSV-1 and 2: molecular basis of HSV latency and reactivation

from Part III - Pathogenesis, clinical disease, host response, and epidemiology: HSV-1 and HSV-2

Published online by Cambridge University Press:  24 December 2009

By
Chris M. Preston  and
Stacey Efstathiou
Edited by
Ann Arvin ,
Gabriella Campadelli-Fiume ,
Edward Mocarski ,
Patrick S. Moore ,
Bernard Roizman ,
Richard Whitley  and
Koichi Yamanishi
Chris M. Preston
Affiliation:
Medical Research Council Virology Unit, Scotland, UK
Stacey Efstathiou
Affiliation:
Division of Virology, Department of Pathology, University of Cambridge, UK
Ann Arvin
Affiliation:
Stanford University, California
Gabriella Campadelli-Fiume
Affiliation:
Università degli Studi, Bologna, Italy
Edward Mocarski
Affiliation:
Emory University, Atlanta
Patrick S. Moore
Affiliation:
University of Pittsburgh
Bernard Roizman
Affiliation:
University of Chicago
Richard Whitley
Affiliation:
University of Alabama, Birmingham
Koichi Yamanishi
Affiliation:
University of Osaka, Japan
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Summary

Introduction

Primary infection with HSV-1 or HSV-2 results in productive replication of the virus at the site of infection, following the pattern of gene expression described elsewhere in this volume. During this initial phase, virus enters sensory neurons via their termini and retrograde transport takes the genome to the neuronal nuclei in the sensory ganglia that innervate the infected dermatome. At early times after infection, virus replication occurs in ganglionic neurons but within a few days no virus can be detected. The genome, however, persists in neurons in a latent state from which it reactivates periodically to resume replication and produce infectious virus. This reactivation event may be “spontaneous” but is generally thought to be provoked by stress stimuli that act on the neuron, or at a peripheral site innervated by the infected ganglion, or systemically. Three phases of latency are recognized. Establishment occurs during the period following primary infection, and although virus replication can be detected in a proportion of neurons during this phase, the initiation and normal progression of productive infection and cell death is arrested in those neurons destined to become latently infected. Unravelling the way in which the seemingly inexorable progression of the gene expression program is blocked constitutes a major challenge for the molecular virologist. The maintenance phase of latency is characterized by the lifelong retention of the HSV genome in a silent state, characterized by repression of all viral lytic genes. One region, encoding the latency-associated transcripts (LATs), remains active during latency.

Type
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Information
Human Herpesviruses
Biology, Therapy, and Immunoprophylaxis
 , pp. 602 - 615
Publisher: Cambridge University Press
Print publication year: 2007

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