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52 - Immunobiology and host response to KSHV infection

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

Published online by Cambridge University Press:  24 December 2009

By
Dimitrios Lagos  and
Chris Boshoff
Edited by
Ann Arvin ,
Gabriella Campadelli-Fiume ,
Edward Mocarski ,
Patrick S. Moore ,
Bernard Roizman ,
Richard Whitley  and
Koichi Yamanishi
Dimitrios Lagos
Affiliation:
Cancer Research UK Viral Oncology Group, Wolfson Institute for Biomedical Research, University College London, London, UK
Chris Boshoff
Affiliation:
Cancer Research UK Viral Oncology Group, Wolfson Institute for Biomedical Research, University College London, London, 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

The interplay between malignancy, infection and immunity is best illustrated by the neoplasms related to KSHV (Boshoff and Weiss, 2002): Kaposi sarcoma (KS) is approximately 100 times more common during immunosuppression and can be resolved when iatrogenic immunosuppression is stopped (Euvrard et al., 2003) and during highly active antiretroviral treatment (HAART) of HIV-1 infected individuals (Boshoff and Weiss, 2002). Primary effusion lymphoma (PEL) and plasmablastic multicentric Castleman's disease (MCD) also occur predominantly during immunosuppression. Like other gammaherpesviruses, KSHV persists as a latent episome in B-lymphocytes (Ambroziak et al., 1995; Cesarman et al., 1995; Renne et al., 1996), without provoking host responses that would eliminate infected cells. KSHV acquired a fascinating repertoire of decoys to trick the host immune response enabling establishment of lifelong infection in humans with very few clinical manifestations. When the balance between viral infection and host immunity is disturbed, some of the molecular pathways employed by KSHV to evade host immune responses are directly involved in driving oncogenesis (Moore and Chang, 2003). KSHV is an excellent model to study the coevolution of pathogen attack and mechanisms of host counter attack.

KS is most aggressive in the immunosuppressed and resolves with partial restoration of the immune system (Gill et al., 2002). Since the introduction of HAART, there has also been a dramatic fall in the incidence of KS (Jacobson et al., 1999).

Type
Chapter
Information
Human Herpesviruses
Biology, Therapy, and Immunoprophylaxis
 , pp. 915 - 928
Publisher: Cambridge University Press
Print publication year: 2007

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