Potential Antigenic Targets on Epstein - Barr Virus-Associated Tumours and the Host Response

  1. Derek J. Chadwick Organizer and
  2. Joan Marsh
  1. D. J. Moss,
  2. S. R. Burrows,
  3. A. Suhrbier and
  4. R. Khanna

Published Online: 28 SEP 2007

DOI: 10.1002/9780470514672.ch2

Ciba Foundation Symposium 187 - Vaccines Against Virally Induced Cancers

Ciba Foundation Symposium 187 - Vaccines Against Virally Induced Cancers

How to Cite

Moss, D. J., Burrows, S. R., Suhrbier, A. and Khanna, R. (2007) Potential Antigenic Targets on Epstein - Barr Virus-Associated Tumours and the Host Response, in Ciba Foundation Symposium 187 - Vaccines Against Virally Induced Cancers (eds D. J. Chadwick and J. Marsh), John Wiley & Sons, Ltd., Chichester, UK. doi: 10.1002/9780470514672.ch2

Author Information

  1. Queensland Institute of Medical Research, The Bancroft Centre, 300 Herston Rd, Brisbane, Queensland 4029, Australia

Publication History

  1. Published Online: 28 SEP 2007

ISBN Information

Print ISBN: 9780471950264

Online ISBN: 9780470514672

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Keywords:

  • potential antigenic targets;
  • epstein-barr virus-associated tumours;
  • host response;
  • immunosuppressed patients;
  • human pathogens

Summary

There is considerable variation in the degree of expression of viral genes among different tumours associated with Epstein-Barr virus (EBV). Immune control of tumours in immunosuppressed patients (immunoblastic lymphomas) can be exercised through a range of epitopes from cytotoxic T lymphocytes (CTL) covering the full spectrum of latent EBV gene products. A subunit vaccine based on an EBV CTL epitope from one of the latent genes is about to undergo human trial. The options for immune control of Burkitt's lymphoma are more restricted. Antigen expression is limited to a single nuclear antigen, EBNA1, and Burkitt's lymphoma cells are unable to process EBV latent antigens, presumably because of a transcriptional defect in TAP1 and TAP2 genes. In contrast with earlier suggestions that EBNA1 is not a target for CTL, there is a class II-restricted epitope within EBNA1. EBV-infected B cells are unable to process this epitope endogenously. The most promising strategy for developing a vaccine against these tumours is to use a single subunit vaccine that incorporates multiple CTL epitopes from several human pathogens.