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The scope of viral causation of human cancers: interpreting virus density from an evolutionary perspective
Paul W Ewald1, Holly A Swain Ewald1
1Department of Biology, University of Louisville , Louisville, KY 40292 , USA.
Abstract:
Most known oncogenic viruses of humans use DNA as their genomic material. Research over the past quarter century has revealed that their oncogenicity results largely from direct interference with barriers to oncogenesis. In contrast to viruses that have been accepted causes of particular cancers, candidate viral causes tend to have fewer viral than cellular genomes in the tumours. These low viral loads have caused researchers to conclude that the associated viruses are not primary causes of the associated cancers. Consideration of differential survival, reproduction and infiltration of cells in a tumour suggest, however, that viral loads could be low even when viruses are primary causes of cancer. Resolution of this issue has important implications for human health because medical research tends to be effective at preventing and controlling infectious diseases. Mathematical models may clarify the problem and help guide future research by assessing whether low viral loads are likely outcomes of the differential survival, reproduction, and infiltration of cells in a tumour and, more generally, the extent to which viruses contribute to cancer. This article is part of the theme issue 'Silent cancer agents: multi-disciplinary modelling of human DNA oncoviruses'.
Insights
Most human cancer-causing viruses are DNA viruses that disrupt cancer barriers. Low viral loads in tumors may still indicate a primary viral role in cancer, challenging current assumptions.
Area of Science:
- Oncology
- Virology
- Mathematical Biology
Background:
- Known human oncogenic viruses primarily utilize DNA genomes.
- Their oncogenicity often stems from direct interference with cellular barriers to cancer development.
- Candidate oncogenic viruses frequently exhibit lower viral genome loads compared to cellular genomes in tumors.
Purpose of the Study:
- To investigate whether low viral loads in tumors can be consistent with viruses being primary causes of cancer.
- To explore the implications of viral load interpretation for understanding infectious disease's role in cancer.
- To assess the utility of mathematical modeling in resolving the role of viruses in oncogenesis.
Main Methods:
- Review of existing research on oncogenic viruses and cancer.
- Consideration of cellular dynamics within tumors, including differential survival, reproduction, and infiltration.
- Proposal for the application of mathematical models to analyze viral contributions to cancer.
Main Results:
- Current research often interprets low viral loads as evidence against a primary causal role for candidate oncogenic viruses.
- Theoretical considerations suggest low viral loads do not necessarily exclude viruses as primary cancer drivers.
- Mathematical modeling is proposed as a tool to rigorously assess this hypothesis.
Conclusions:
- The interpretation of low viral loads in tumors requires careful consideration of cellular dynamics.
- Viruses may be primary causes of cancer even with low observed viral loads.
- Mathematical modeling can provide crucial insights into the role of viruses in cancer etiology and guide future research.
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