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Arbovirus Infections As Screening Tools for the Identification of Viral Immunomodulators and Host Antiviral Factors
Published on: September 13, 2018
When Viruses Cross Developmental Pathways
Pankaj Trivedi1, Sandesh Kumar Patel2, Diana Bellavia2
1Department of Experimental Medicine, Sapienza University of Rome, Rome, Italy.
Abstract:
Aberrant regulation of developmental pathways plays a key role in tumorigenesis. Tumor cells differ from normal cells in their sustained proliferation, replicative immortality, resistance to cell death and growth inhibition, angiogenesis, and metastatic behavior. Often they acquire these features as a consequence of dysregulated Hedgehog, Notch, or WNT signaling pathways. Human tumor viruses affect the cancer cell hallmarks by encoding oncogenic proteins, and/or by modifying the microenvironment, as well as by conveying genomic instability to accelerate cancer development. In addition, viral immune evasion mechanisms may compromise developmental pathways to accelerate tumor growth. Viruses achieve this by influencing both coding and non-coding gene regulatory pathways. Elucidating how oncogenic viruses intersect with and modulate developmental pathways is crucial to understanding viral tumorigenesis. Many currently available antiviral therapies target viral lytic cycle replication but with low efficacy and severe side effects. A greater understanding of the cross-signaling between oncogenic viruses and developmental pathways will improve the efficacy of next-generation inhibitors and pave the way to more targeted antiviral therapies.
Insights
Oncogenic viruses disrupt developmental pathways, driving cancer. Understanding these viral interactions can lead to more effective, targeted antiviral therapies with fewer side effects.
Area of Science:
- Oncology
- Virology
- Molecular Biology
Background:
- Aberrant regulation of developmental pathways is fundamental to tumorigenesis.
- Tumor cells exhibit hallmarks like sustained proliferation and metastasis, often due to dysregulated Hedgehog, Notch, or WNT signaling.
- Human tumor viruses contribute to cancer by encoding oncogenic proteins, altering the microenvironment, and inducing genomic instability.
Purpose of the Study:
- To elucidate the mechanisms by which oncogenic viruses intersect with and modulate developmental pathways.
- To understand the role of viral immune evasion in accelerating tumor growth via developmental pathway compromise.
- To identify targets for improved antiviral therapies by exploring virus-developmental pathway cross-signaling.
Main Methods:
- Review of literature on oncogenic viruses and developmental pathway regulation.
- Analysis of viral oncogenic proteins and their impact on cellular signaling.
- Investigation of viral modulation of coding and non-coding gene regulatory pathways.
Main Results:
- Oncogenic viruses can hijack developmental pathways (Hedgehog, Notch, WNT) to promote cancer hallmarks.
- Viral immune evasion strategies can further dysregulate developmental pathways, accelerating tumor progression.
- Current antiviral therapies targeting viral replication show limited efficacy and significant side effects.
Conclusions:
- Elucidating virus-developmental pathway interactions is critical for understanding viral tumorigenesis.
- Targeting the cross-signaling between oncogenic viruses and developmental pathways offers a promising strategy for next-generation antiviral therapies.
- A deeper understanding will enable the development of more targeted and effective antiviral treatments with improved safety profiles.
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