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62 - Herpesvirus evasion of T-cell immunity

from Part V - Subversion of adaptive immunity

Published online by Cambridge University Press:  24 December 2009

Benjamin E. Gewurz
Affiliation:
Department of Pathology, Harvard Medical School, Boston, MA, USA
Jatin M. Vyas
Affiliation:
Division of Infectious Disease, Department of Medicine, Massachusetts General Hospital, Boston, MA, USA
Hidde L. Ploegh
Affiliation:
Department of Pathology, Harvard Medical School, Boston, 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

The multiple layers of the human immune response present a challenge to viruses, which must survive and multiply within a host for a sufficient period of time to allow successful transmission to susceptible individuals. Given the large proteomes and comparatively low polymerase error rate of human herpesviruses, antiviral immunity at first glance appear to have the upper hand. Nonetheless, herpesviruses manage prolonged incubation periods following initial infection, with systemic dissemination and prolonged secretion, often from multiple sites. In contrast to the similarly large poxviruses, the ability to subsequently establish persistent infection is a hallmark of the human herpesviruses. To enable this lifestyle, the herpesviruses devote a significant proportion of their genome coding capacity to the expression of immuno-evasins, a collection of molecules that disrupt normal immune physiology. Each human herpesvirus studied has evolved elegant cell biological solutions to problems posed by the immune response.

Innate immunity, an evolutionarily conserved and relatively non-specific system of pattern recognition molecules hardwired in the genome, cytokines such as interferons, phagocytes and natural killer (NK) cells, represents the first line deployed against microbial invaders, including herpesviruses (Janeway and Medzhitov, 2002). The clonal expansion of B- and T- lymphocytes that bear antigen-specific receptors for viral epitopes underlies the adaptive antiviral immune response, laying the groundwork for a highly pathogen-specific defense. Such specificity comes at a price – lymphocyte proliferation requires time to unfold, and innate immunity, in particular NK-cell activity, limits the initial herpesvirus spread.

Type
Chapter
Information
Human Herpesviruses
Biology, Therapy, and Immunoprophylaxis
, pp. 1117 - 1136
Publisher: Cambridge University Press
Print publication year: 2007

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