Mechanisms of Cross-Protection between Plant Virus Strains

  1. David Evered Organizer,
  2. Sara Harnett
  1. John L. Sherwood

Published Online: 28 SEP 2007

DOI: 10.1002/9780470513569.ch10

Ciba Foundation Symposium 133 - Plant Resistance to Virus

Ciba Foundation Symposium 133 - Plant Resistance to Virus

How to Cite

Sherwood, J. L. (2007) Mechanisms of Cross-Protection between Plant Virus Strains, in Ciba Foundation Symposium 133 - Plant Resistance to Virus (eds D. Evered and S. Harnett), John Wiley & Sons, Ltd., Chichester, UK. doi: 10.1002/9780470513569.ch10

Author Information

  1. Oklahoma State University, Department of Plant Pathology, Division of Agriculture, Life Sciences East 104, Stillwater, Oklahoma 74078-0285, USA

Publication History

  1. Published Online: 28 SEP 2007

ISBN Information

Print ISBN: 9780471912637

Online ISBN: 9780470513569

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Keywords:

  • cross-protection;
  • plant virus strains;
  • genome-length viral nucleic acid;
  • dark green agent;
  • specific metabolite utilization

Summary

Cross-protection (the phenomenon whereby the activity of a virus in a plant prevents the expression of a subsequent challenge virus) has been used successfully to control some virus diseases. Mechanisms to account for specificity have been proposed that operate either at the initial interaction between the plant infected with the protecting virus and the challenge virus, or during the replication of the challenge virus. In the initial interaction, the challenge virus could be inhibited from uncoating, thereby preventing the initiation of the replicative cycle. If replication is initiated, a number of mechanisms may be involved in controlling replication of the challenge virus: (1) the initial translation of the incoming viral nucleic acid could be blocked, (2) the transcription of the incoming viral nucleic acid may be prevented even if it is translated initially, and (3) the production of genome-length viral nucleic acid could be inhibited. Finally, even if challenge virus is replicated, movement from cell to cell could be prevented. Explanation of cross-protection by one hypothesis alone is unlikely because of the contrasting observations in a variety of biological systems. However, it is plausible that different mechanisms of cross-protection may be operating in different virus groups.