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Updated: Oct 4, 2025

Paramyxoviruses for Tumor-targeted Immunomodulation: Design and Evaluation Ex Vivo
Published on: January 7, 2019
Oncogenic Viruses as Entropic Drivers of Cancer Evolution
Italo Tempera1, Paul M Lieberman1
1Program in Gene Expression and Regulation, The Wistar Institute, Philadelphia, PA, United States.
Abstract:
Viral infection is an indisputable causal factor for nearly 17% of all human cancers. However, the diversity and complexity of oncogenic mechanisms raises new questions as to the mechanistic role of viruses in cancer. Classical viral oncogenes have been identified for all tumor-associated viruses. These oncogenes can have multiple oncogenic activities that may or may not be utilized in a particular tumor cell. In addition, stochastic events, like viral mutation and integration, as well as heritable host susceptibilities and immune deficiencies are also implicated in tumorigenesis. A more contemporary view of tumor biology highlights the importance of evolutionary forces that select for phenotypes better adapted to a complex and changing environment. Given the challenges of prioritizing singular mechanistic causes, it may be necessary to integrate concepts from evolutionary theory and systems biology to better understand viral cancer-driving forces. Here, we propose that viral infection provides a biological "entropy" that increases genetic variation and phenotypic plasticity, accelerating the main driving forces of cancer cell evolution. Viruses can also influence the evolutionary selection criteria by altering the tumor microenvironment and immune signaling. Utilizing concepts from cancer cell evolution, population genetics, thermodynamics, and systems biology may provide new perspectives on viral oncogenesis and identify novel therapeutic strategies for treating viruses and cancer.
Insights
Viral infections contribute to 17% of human cancers. This study proposes viruses act as a biological "entropy" source, accelerating cancer cell evolution and suggesting new therapeutic strategies.
Area of Science:
- Oncology
- Virology
- Evolutionary Biology
- Systems Biology
Background:
- Viral infections are linked to approximately 17% of human cancers.
- The precise mechanisms by which viruses drive oncogenesis are complex and not fully understood.
- Traditional models focus on viral oncogenes, but other factors like host genetics and immune status also play roles.
Purpose of the Study:
- To explore the role of evolutionary forces and systems biology in understanding viral oncogenesis.
- To propose a novel framework viewing viral infection as a source of biological "entropy" that promotes cancer evolution.
- To identify potential new therapeutic strategies by integrating concepts from cancer evolution and virology.
Main Methods:
- Literature review and conceptual synthesis integrating evolutionary theory, systems biology, and cancer research.
- Analysis of oncogenic mechanisms, including viral mutation, integration, host susceptibility, and immune interactions.
- Application of principles from population genetics and thermodynamics to cancer cell evolution.
Main Results:
- Viral infections can increase genetic variation and phenotypic plasticity, accelerating cancer cell evolution.
- Viruses influence tumor microenvironment and immune signaling, altering cancer cell selection criteria.
- A systems biology approach reveals viruses as key drivers of cancer evolution through increased biological entropy.
Conclusions:
- Viewing viral oncogenesis through the lens of evolutionary theory and systems biology offers new insights.
- Viral infections can be conceptualized as a source of biological entropy, promoting cancer development.
- Integrating diverse biological concepts may lead to novel therapeutic strategies for virus-associated cancers.
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