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56 - KSHV-induced oncogenesis

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

Published online by Cambridge University Press:  24 December 2009

By
Donald Ganem
Edited by
Ann Arvin ,
Gabriella Campadelli-Fiume ,
Edward Mocarski ,
Patrick S. Moore ,
Bernard Roizman ,
Richard Whitley  and
Koichi Yamanishi
Donald Ganem
Affiliation:
Howard Hughes Medical Institute, Departments of Microbiology and Immunology and Medicine, University of California, San Francisco, CA, 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

Human infection by KSHV is associated with the development of at least three proliferative disorders: Kaposi's sarcoma (KS), primary effusion lymphoma (PEL) and a subset of multicentric Castleman's disease (MCD). In keeping with the classification of KSHV as a lymphotropic (γ2) herpesvirus, two of these (PEL and MCD) are primary disorders of the B cell lineage. The third, KS, is a more complex lesion driven by proliferation of cells of endothelial lineage. KSHV is the second human γ-herpesvirus to be linked to neoplasia (EBV being the first). As such, many notions about how KSHV engenders these lesions have been heavily influenced by paradigms derived from the study of EBV-induced malignancies. In EBV, the viral latency program is powerfully immortalizing in vitro, and is thought to be the principal genetic program driving virus-related tumorigenesis. Lytic infection, while presumed important for dissemination of infection to target cells early in infection (and following lytic reactivation at later times), is not thought to play a direct role in the histogenesis of the tumors. As we shall see, although many parallels indeed exist with EBV, the distinctive features of the KSHV-associated diseases makes routine extrapolation from other viral models an enterprise to be undertaken with caution. In this chapter, we will review the biology of the KSHV-associated malignancies and consider the cellular and molecular mechanisms by which KSHV infection contributes to their pathogenesis.

Primary effusion lymphoma (PEL)

PEL is a classical neoplasm involving cells of the B cell lineage (see review by Cesarman, this volume).

Type
Chapter
Information
Human Herpesviruses
Biology, Therapy, and Immunoprophylaxis
 , pp. 1007 - 1028
Publisher: Cambridge University Press
Print publication year: 2007

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To save content items to your account, please confirm that you agree to abide by our usage policies. If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account. Find out more about saving content to Dropbox.

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Save book to Google Drive

To save content items to your account, please confirm that you agree to abide by our usage policies. If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account. Find out more about saving content to Google Drive.

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