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Within- and between-host evolutionary effects on viral oncogenicity.

Yoshiki Koizumi1,2, Michael B Bonsall1

  • 1Department of Biology, University of Oxford, South Parks Road, Oxford OX1 3RB, United Kingdom.

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Summary
This summary is machine-generated.

Mathematical models reveal how cancer-causing viruses (oncogenic viruses) evolve. Understanding these evolutionary dynamics, particularly cell transformation and proliferation rates, is key to explaining viral diversity and host interactions.

Keywords:
apparent competitionfitness landscapemathematical modellingnested modeloncovirusvirus dynamics

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Area of Science:

  • Evolutionary biology
  • Virology
  • Immunology

Background:

  • Over 10% of cancers are linked to cancer-inducing viruses (oncogenic viruses).
  • The evolutionary pathways by which viruses acquire oncogenic properties are not well understood.
  • Viral oncogenesis involves complex interactions between viruses and the host immune system.

Purpose of the Study:

  • Investigate the evolutionary conditions influencing viral oncogenicity at within- and between-host levels.
  • Model oncovirus-immune system interactions as an extended enemy-victim relationship.
  • Examine how oncogenic traits affect within-host viral dynamics, including cell transformation and proliferation rates.

Main Methods:

  • Utilized mathematical modeling to simulate oncovirus-immune system interactions.
  • Analyzed the impact of transformation rate of infected cells into pre-cancerous states.
  • Assessed pre-cancerous cell proliferation rate under various within-host conditions.

Main Results:

  • Identified transformation and proliferation rates that maximize viral fitness within and between hosts.
  • Found that the optimal transformation rate depends on viral production, immunogenicity, and immune elimination of pre-cancerous cells.
  • Observed that intermediate proliferation rates can minimize viral fitness, potentially explaining the diversity of oncogenic viruses.

Conclusions:

  • Provided insights into the evolutionary drivers of viral oncogenicity.
  • Highlighted the intricate interplay between oncogenic viruses and host immune responses.
  • Offered explanations for the observed diversity among oncogenic viruses.