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31 - Human gammaherpesvirus immune evasion strategies

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

Published online by Cambridge University Press:  24 December 2009

By
Robert E. Means ,
Sabine M. Lang  and
Jae U. Jung
Edited by
Ann Arvin ,
Gabriella Campadelli-Fiume ,
Edward Mocarski ,
Patrick S. Moore ,
Bernard Roizman ,
Richard Whitley  and
Koichi Yamanishi
Robert E. Means
Affiliation:
Department of Pathology, Yale University School of Medicine, New Haven, CT, USA
Sabine M. Lang
Affiliation:
Department of Pathology, Yale University School of Medicine, New Haven, CT, USA
Jae U. Jung
Affiliation:
Division of Tumor Virology, New England Primate Research Center, Harvard Medical School, Southborough, MA, 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

The human γ-HVs are able to establish a lifelong, persistent infection that is largely clinically inapparent within the immunocompetent host. However, when these viruses are not kept in check, a variety of lymphoproliferative and neoplastic disorders result that will be detailed elsewhere within this volume. In brief, for HHV-8, also known as Kaposi's sarcoma-associated herpesvirus (KSHV), these neoplasias include Kaposi's sarcoma (KS), multicentric Castleman's disease (MCD) and primary effusion lymphoma (PEL). HHV-4, or Epstein–Barr virus (EBV), has been etiologically associated with infectious mononucleosis, Burkitt's lymphoma, nasopharyngeal carcinoma (NPC), Hodgkin's disease, hemophagocytic lymphohistiocytosis syndrome and some gastric cancers. Through coevolution with their hosts, these viruses have acquired a number of genes that act to set a fine balance between the uncontrolled, virally driven cellular proliferation seen in the immunocompromised host and complete elimination of infected cells by the immune responses. Several of these gene products cause selective suppression of normal immune system functioning and allow for an apathogenic, persistent infection.

Immune system overview

The immune system provides multiple mechanisms of protection from invading pathogens, whether viral, bacterial or parasitic. These immune responses include both broad spectrum, innate responses and highly specific, adaptive responses. Mechanisms of the innate response include the production of viral replication blocking interferons, opsonization and lysis by the complement cascade and natural antibodies, apoptosis, as well as clearance of infection by natural killer (NK) cells, macrophages, neutrophils and T-cells.

Type
Chapter
Information
Human Herpesviruses
Biology, Therapy, and Immunoprophylaxis
 , pp. 559 - 586
Publisher: Cambridge University Press
Print publication year: 2007

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