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24 - Gammaherpesvirus maintenance and replication during latency

from Part II - Basic virology and viral gene effects on host cell functions: gammaherpesviruses

Published online by Cambridge University Press:  24 December 2009

By
Paul M. Lieberman ,
Jianhong Hu  and
Rolf Renne
Edited by
Ann Arvin ,
Gabriella Campadelli-Fiume ,
Edward Mocarski ,
Patrick S. Moore ,
Bernard Roizman ,
Richard Whitley  and
Koichi Yamanishi
Paul M. Lieberman
Affiliation:
The Wistar Institute, Philadelphia, PA
Jianhong Hu
Affiliation:
University of Florida, Gainesville, FL
Rolf Renne
Affiliation:
University of Florida, Gainesville, FL
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

The human gammaherpesviruses Epstein–Barr Virus (EBV) and Kaposi's sarcoma-associated herpesvirus (KSHV) are associated with a variety of malignancies involving cells of various lineages.

After primary infection and initial viral propagation in epithelial and lymphoid cells, both viruses establish latency in a subset of CD 19 positive B-cells. In this often lifelong asymptomatic stage, in which EBV genomes are detectable primarily in resting memory B-cells, the number of infected cells is extremely low and virus load is tightly controlled by the host cellular and humoral immune response.

Loss of this balance leads to an increase in viral load, which often precedes the onset of malignant diseases. Both tissue involvement and histopathology are highly variable between EBV - and KSHV -associated malignancies and involve either lymphoid (Burkitt's lymphoma and primary effusion lymphoma), epithelial (nasopharyngeal carcinoma), or endothelial (Kaposi's sarcoma) tissues.

However, common to all gammaherpesvirus-associated tumors is that the majority of tumor cells are latently infected, and harbor extrachromosomal circularized viral genomes called episomes that are replicated and segregated by the host cellular replication machinery indefinitely. This ability to maintain long-term latent infection in quiescent and proliferating cells may be a defining property shared by both the lymphocryptoviruses (LCV, represented by EBV) and the rhadinoviruses (RDV, represented by KSHV).

This chapter aims to summarize our current understanding of the underlying mechanisms by which EBV and KSHV achieve long-term episomal maintenance in latently infected cells, which conceptually can be viewed as a two step process: replication of the viral genome and faithful segregation to daughter cells (Fig. 24.1).

Type
Chapter
Information
Human Herpesviruses
Biology, Therapy, and Immunoprophylaxis
 , pp. 379 - 402
Publisher: Cambridge University Press
Print publication year: 2007

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