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51 - EBV: Immunobiology and host response

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

Published online by Cambridge University Press:  24 December 2009

By
Denis J. Moss ,
Scott R. Burrows  and
Rajiv Khanna
Edited by
Ann Arvin ,
Gabriella Campadelli-Fiume ,
Edward Mocarski ,
Patrick S. Moore ,
Bernard Roizman ,
Richard Whitley  and
Koichi Yamanishi
Denis J. Moss
Affiliation:
Infectious Disease and Immunology Division, Queensland Institute of Medical Research and Joint Oncology Program, University of Queensland, Australia
Scott R. Burrows
Affiliation:
Infectious Disease and Immunology Division, Queensland Institute of Medical Research and Joint Oncology Program, University of Queensland, Australia
Rajiv Khanna
Affiliation:
Infectious Disease and Immunology Division, Queensland Institute of Medical Research and Joint Oncology Program, University of Queensland, Australia
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 biology and immunology of Epstein–Barr virus (EBV) has continued to fascinate researchers because the lessons learnt provide a platform for understanding the interplay between the biology of this ubiquitous infection, the immune system seeking to restrict its spread and the emergence of a variety of malignancies. As with other gamma herpes viruses, EBV encodes a large set of lytic cycle genes together with a number of latent genes which are associated with expansion of the latent EBV pool in B-lymphocytes. Current evidence suggests that the virus gains entry into the body by infection of B-lymphocytes in the oral cavity via an interaction between the major viral glycoprotein gp340 and the complement receptor CR2 which is expressed on B-cells, although a role for CR2-expressing or non-expressing epithelial and/or T-cells cannot be totally discounted. In either case, evidence suggests that the earliest detectable event following primary infection is the expression of lytic cycle proteins resulting in the release of infectious virus into the oral cavity followed by a generalized seeding of latently infected B-lymphocytes throughout the body. This primary infection results in symptoms of acute infectious mononucleosis (IM) in about 50% of adolescents and is coincident with a marked lymphocytosis (dominated by EBV-specific cytotoxic T-cells) and the appearance of an IgM response to a variety of EBV proteins, most notably the viral capsid antigen, VCA.

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Human Herpesviruses
Biology, Therapy, and Immunoprophylaxis
 , pp. 904 - 914
Publisher: Cambridge University Press
Print publication year: 2007

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References

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  • EBV: Immunobiology and host response
    • By Denis J. Moss, Infectious Disease and Immunology Division, Queensland Institute of Medical Research and Joint Oncology Program, University of Queensland, Australia, Scott R. Burrows, Infectious Disease and Immunology Division, Queensland Institute of Medical Research and Joint Oncology Program, University of Queensland, Australia, Rajiv Khanna, Infectious Disease and Immunology Division, Queensland Institute of Medical Research and Joint Oncology Program, University of Queensland, Australia
  • Edited by Ann Arvin, Stanford University, California, Gabriella Campadelli-Fiume, Università degli Studi, Bologna, Italy, Edward Mocarski, Emory University, Atlanta, Patrick S. Moore, University of Pittsburgh, Bernard Roizman, University of Chicago, Richard Whitley, University of Alabama, Birmingham, Koichi Yamanishi, University of Osaka, Japan
  • Book: Human Herpesviruses
  • Online publication: 24 December 2009
  • Chapter DOI: https://doi.org/10.1017/CBO9780511545313.052
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  • EBV: Immunobiology and host response
    • By Denis J. Moss, Infectious Disease and Immunology Division, Queensland Institute of Medical Research and Joint Oncology Program, University of Queensland, Australia, Scott R. Burrows, Infectious Disease and Immunology Division, Queensland Institute of Medical Research and Joint Oncology Program, University of Queensland, Australia, Rajiv Khanna, Infectious Disease and Immunology Division, Queensland Institute of Medical Research and Joint Oncology Program, University of Queensland, Australia
  • Edited by Ann Arvin, Stanford University, California, Gabriella Campadelli-Fiume, Università degli Studi, Bologna, Italy, Edward Mocarski, Emory University, Atlanta, Patrick S. Moore, University of Pittsburgh, Bernard Roizman, University of Chicago, Richard Whitley, University of Alabama, Birmingham, Koichi Yamanishi, University of Osaka, Japan
  • Book: Human Herpesviruses
  • Online publication: 24 December 2009
  • Chapter DOI: https://doi.org/10.1017/CBO9780511545313.052
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  • EBV: Immunobiology and host response
    • By Denis J. Moss, Infectious Disease and Immunology Division, Queensland Institute of Medical Research and Joint Oncology Program, University of Queensland, Australia, Scott R. Burrows, Infectious Disease and Immunology Division, Queensland Institute of Medical Research and Joint Oncology Program, University of Queensland, Australia, Rajiv Khanna, Infectious Disease and Immunology Division, Queensland Institute of Medical Research and Joint Oncology Program, University of Queensland, Australia
  • Edited by Ann Arvin, Stanford University, California, Gabriella Campadelli-Fiume, Università degli Studi, Bologna, Italy, Edward Mocarski, Emory University, Atlanta, Patrick S. Moore, University of Pittsburgh, Bernard Roizman, University of Chicago, Richard Whitley, University of Alabama, Birmingham, Koichi Yamanishi, University of Osaka, Japan
  • Book: Human Herpesviruses
  • Online publication: 24 December 2009
  • Chapter DOI: https://doi.org/10.1017/CBO9780511545313.052
Available formats
×