Evasion of Host Immune Responses by Tumours and Viruses

  1. Derek J. Chadwick Organizer and
  2. Joan Marsh
  1. Peter C. Doherty1,
  2. Ralph A. Tripp1 and
  3. John W. Sixbey2

Published Online: 28 SEP 2007

DOI: 10.1002/9780470514672.ch16

Ciba Foundation Symposium 187 - Vaccines Against Virally Induced Cancers

Ciba Foundation Symposium 187 - Vaccines Against Virally Induced Cancers

How to Cite

Doherty, P. C., Tripp, R. A. and Sixbey, J. W. (2007) Evasion of Host Immune Responses by Tumours and Viruses, 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.ch16

Author Information

  1. 1

    Department of Immunology, St Jude Children's Research Hospital, University of Tennessee, 332 North Lauderdale, PO Box 318, Memphis, TN 38104, USA

  2. 2

    Virology and Molecular Biology, St Jude Children's Research Hospital, 332 North Lauderdale, Memphis, TN 38104, USA

Publication History

  1. Published Online: 28 SEP 2007

ISBN Information

Print ISBN: 9780471950264

Online ISBN: 9780470514672

SEARCH

Keywords:

  • evasion;
  • host immune responses;
  • tumours;
  • viruses;
  • basal epithelia

Summary

Viruses and tumours use various mechanisms to avoid immune surveillance. Oncogenic viruses have achieved a balance with the immune system through evolutionary time to ensure long-term persistence. Mutations that promote escape mechanisms favouring tumour growth to the detriment of host survival through reproductive age offer no selective advantage and will not generally be maintained in the viral genome that persists in nature. Conventional (non-oncogenic) and tumour viruses interact with various immune mediators and T cells in different ways. Oncogenic viruses cannot operate solely in the context of a lytic cycle, though this may be characteristic of the initial phase of infection that is limited by the acute immune response. Some oncogenic viruses interact with normal cellular growth control and signalling mechanisms. Synthesis of key viral proteins may be tightly controlled in replicating cells that are subject to T cell surveillance, such as basal epithelia, while productive infection occurs in non-proliferating progeny that are lost under normal physiological conditions, such as desquamating epithelia. Tumorigenesis may be an aberrant consequence of the molecular mechanisms needed to maintain this pattern of viral growth regulation in the context of the cell cycle. Vaccines designed to limit the acute phase of infection with cell-free oncogenic viruses should be as effective as those for conventional viruses.