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26 - Reactivation and lytic replication of KSHV

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

Published online by Cambridge University Press:  24 December 2009

By
David M. Lukac  and
Yan Yuan
Edited by
Ann Arvin ,
Gabriella Campadelli-Fiume ,
Edward Mocarski ,
Patrick S. Moore ,
Bernard Roizman ,
Richard Whitley  and
Koichi Yamanishi
David M. Lukac
Affiliation:
UMDNJ/NJ Medical School, Dept. of Microbiology and Molecular Genetics, Newark, NJ, USA
Yan Yuan
Affiliation:
University of Pennsylvania School of Dental Medicine, Dept. of Microbiology, Philadelphia, PA, 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

Overview: goals of lytic replication

Herpesviruses are extremely successful pathogens that have coevolved with their mammalian hosts over the past 60–80 million years (McGeoch and Davison, 1999). This success likely is attributable to the ability of the Herpesviridae to establish lifelong latent infections of their host. Latently infected cells provide a perpetual reservoir from which progeny viruses can be amplified for dissemination within the host and transmission between hosts. Herpesvirologists have traditionally used the term “lytic reactivation” to describe the biological events that begin with emergence of a virus from latency and end with lysis of the host cell and release of progeny virions. Clinico-epidemiologic studies suggest that lytic reactivation of KSHV is an essential pathogenic step in multiple human diseases. The goal of this chapter is to review the host–virus interactions that are critical for regulating induction of KSHV from latency, subsequent progression through the lytic cycle, replication of the viral genome, and assembly of mature viral particles.

Lytic reactivation of KSHV is a critical pathogenic step in development of KS and other human diseases

Numerous epidemiologic studies unanimously agree that reactivation of KSHV from latency is a critical pathogenic step during the progression to KS. Serologic assays (Gao et al., 1996a; Kedes et al., 1996; Martin et al., 1998; Simpson et al., 1996) demonstrate that primary infection by KSHV typically occurs at least 10 years prior to clinically apparent KS in AIDS patients (Martin et al., 1998).

Type
Chapter
Information
Human Herpesviruses
Biology, Therapy, and Immunoprophylaxis
 , pp. 434 - 460
Publisher: Cambridge University Press
Print publication year: 2007

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