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42 - HCMV: molecular basis of persistence and latency

from Part III - Pathogenesis, clinical disease, host response, and epidemiology: HCMV

Published online by Cambridge University Press:  24 December 2009

By
Michael A. Jarvis  and
Jay A. Nelson
Edited by
Ann Arvin ,
Gabriella Campadelli-Fiume ,
Edward Mocarski ,
Patrick S. Moore ,
Bernard Roizman ,
Richard Whitley  and
Koichi Yamanishi
Michael A. Jarvis
Affiliation:
Vaccine and Gene Therapy Institute, Oregon Health Science University, Portland, OR, USA
Jay A. Nelson
Affiliation:
Department of Molecular Microbiology and Immunology, Oregon Health Sciences University, Portland, OR, USA
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

Human cytomegalovirus (HCMV) is an ubiquitous β-herpesvirus that establishes a lifelong infection within the host. Although HCMV is generally asymptomatic within the normal individual, the virus causes severe and incapacitating disease in immune compromised patients (Pass, 2001). A critical component for HCMV persistence in the non-immune compromised host is the ability of the virus to establish cellular sites of latency as well as persistent infection. During latency, the HCMV genome is maintained within the cell with limited viral gene expression reactivating virus upon cellular stimulation. In HCMV persistent infection, infectious virus is continually produced in the cell with minimal cytopathic effect thereby enabling long-term infection. Endothelial cells (ECs) and specific subpopulations of the myeloid lineage are believed to represent important sites of persistent HCMV replication and latency, respectively. Recent studies of HCMV and the closely related murine cytomegalovirus (MCMV) are beginning to identify the virally encoded genetic determinants required for replication in these cell types. The establishment of latent infection in myeloid cells that are critical cellular components of the host immune system, also closely interconnects HCMV and the host immune response. This chapter will focus on the role of ECs and myeloid cells as sites of CMV persistent replication and latency, and the viral mechanisms that modulate cellular functions to ensure survival and reactivation within the host.

Type
Chapter
Information
Human Herpesviruses
Biology, Therapy, and Immunoprophylaxis
 , pp. 765 - 779
Publisher: Cambridge University Press
Print publication year: 2007

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