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Efficacy of Immune Checkpoint Inhibitors and Oncoviruses in Solid Tumors
Hiba Mechahougui1,2, Léna Royston3, Catia Vieira Gomes2,4
1Division of Medical Oncology, Geneva University Hospitals, Geneva, Switzerland.
Abstract:
Viral infections are estimated to contribute to 12% to 20% of all cancers worldwide, with virus-driven malignancies disproportionately affecting low- and middle-income countries, whereas metabolic and nonviral factors predominate in high-income regions. Key oncogenic viruses that cause solid tumors include high-risk human papillomaviruses, Epstein-Barr virus, hepatitis B virus, hepatitis C virus, Kaposi sarcoma-associated herpesvirus, and Merkel cell polyomavirus. Immune checkpoint inhibitors (ICI) have revolutionized cancer therapy by boosting immune responses against tumors. Although viral infection-associated tumors often exhibit "hot" immune profiles, clinical outcomes with ICIs remain inconsistent. Some studies report improved survival in virus-associated cancers, whereas others indicate no clear benefit, which might reflect high variability in tumor microenvironments and immune responses. In this review, we aim to explore the direct and indirect contribution of different viruses to carcinogenesis in solid tumors, with a particular focus on immunotherapy effectiveness based on infection status.
Insights
Viral infections contribute to 12-20% of global cancers, particularly in low-income nations. This review examines oncogenic viruses, solid tumors, and the inconsistent effectiveness of immune checkpoint inhibitors (ICIs) in virus-associated cancers.
Area of Science:
- Oncology
- Virology
- Immunotherapy
Background:
- Viral infections are linked to 12-20% of global cancers, with significant disparities between high-income and low-to-middle-income countries.
- Key oncogenic viruses implicated in solid tumors include HPV, EBV, HBV, HCV, KSHV/HHV-8, and MCPyV.
- Immune checkpoint inhibitors (ICIs) have transformed cancer treatment, but their efficacy in virus-associated cancers is variable.
Purpose of the Study:
- To review the direct and indirect roles of various viruses in solid tumor carcinogenesis.
- To analyze the effectiveness of immunotherapy, specifically ICIs, in virus-associated cancers based on infection status.
Main Methods:
- Literature review of studies on viral carcinogenesis and immunotherapy outcomes.
- Analysis of tumor microenvironment and immune response variability in virus-associated cancers.
Main Results:
- Virus-associated tumors often display "hot" immune profiles, suggesting potential ICI responsiveness.
- Clinical outcomes with ICIs in virus-associated cancers show significant inconsistency.
- Variability in tumor microenvironments and immune responses may explain inconsistent ICI benefits.
Conclusions:
- Understanding the interplay between oncogenic viruses and the immune system is crucial for optimizing cancer immunotherapy.
- Further research is needed to elucidate factors driving differential responses to ICIs in virus-driven malignancies.
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