Many cancers are etiologically linked to viral infections, such as Epstein-Barr virus (EBV), hepatitis B and C viruses (HBV/HCV), human papillomavirus (HPV), human immunodeficiency virus (HIV) and others. Viral oncogenesis involves intricate interactions between viral factors and host cellular machinery, profoundly shaping tumor biological behaviors, the surrounding microenvironment, and the immune system. These virus-driven alterations fuel malignant transformation, modulate immune responses, and promote immune evasion and therapeutic resistance. Emerging evidence highlights key mechanisms including immunosuppression, metabolic reprogramming, chronic inflammation, and changes in genomics, genetics and epigenetics, which collectively create unique therapeutic vulnerabilities. Despite advances in immunotherapy, cancer vaccines and targeted therapies, treatment resistance remains a challenge. This Research Topic aims to consolidate cutting-edge research on virus-induced mechanisms across virus-associated cancers to uncover novel vulnerabilities and improve therapeutic outcomes.
It aims to investigate virus-induced mechanisms driving tumorigenesis, immune evasion, and therapeutic resistance across virus-associated cancers, including those linked to EBV, HBV/HCV, HPV, HIV, and others. We focus on the complex molecular interplay involving viral factors, tumor cells, immune cells, stromal components, and the extracellular matrix (ECM) within the microenvironment, lymph nodes and periphery. The primary objective is to deepen understanding of how virus-mediated signaling pathways reshape anti-tumor immune responses and influence clinical outcomes. Specifically, we seek to address the following critical questions:
1. What viral and host-derived mechanisms contribute to immune suppression, tumor progression, and therapeutic resistance in virus-associated cancers? 2. How can virus-associated biomarkers or molecular signatures be leveraged to stratify patients, predict therapeutic responses, and facilitate personalized treatment? 3. What therapeutic vulnerabilities arise from virus-host interactions, and how can these be targeted to enhance the efficacy of existing and emerging modalities, including immunotherapy, targeted therapy, and combination approaches? By integrating state-of-the-art research, this Research Topic aims to elucidate virus-specific oncogenic and immunosuppressive pathways, promoting innovative therapeutic strategies and improving outcomes in virus-driven cancers. We welcome submissions that investigate the diverse landscape of virus-induced mechanisms underlying tumorigenesis, immune modulation, and therapeutic resistance across virus-associated cancers. Authors are encouraged to submit original research, resource articles, comprehensive reviews, and perspectives addressing, but not limited to, the following themes: • Virus-host interactions: Molecular and cellular interplay between oncogenic viruses and host immune or tumor cells, highlighting pathways critical for viral oncogenesis and immune evasion. • Immune modulation in the virus-associated tumor ecosystem: Roles of immune and stromal cell subsets, as well as ECM components, modulated by viral infection. • Virus-driven metabolic reprogramming: How viral infections alter cellular metabolism and impact immune responses and therapeutic responsiveness. • Biomarkers for patient stratification and precision medicine: Viral or host-derived biomarkers, molecular signatures, and immune profiles predictive of therapeutic responses. • Therapeutic vulnerabilities and targets: Novel targets arising from virus-induced pathways, and preclinical or clinical evaluation of strategies exploiting virus–host interactions. • Omics-driven characterization: Integrated omics analyses elucidating viral and molecular landscapes, particularly in the context of immunotherapy and targeted therapies. • Preclinical and clinical evaluations: Translational studies and clinical trials assessing therapies designed to exploit vulnerabilities from virus–host interplay.
By bringing together innovative research across these thematic areas, this Research Topic aims to advance understanding of virus-driven oncogenic mechanisms and therapeutic vulnerabilities, ultimately facilitating improved clinical outcomes for patients with virus-associated cancers.
Please note that manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by robust and relevant validation (clinical cohort or biological validation in vitro or in vivo) are out of scope for this Research Topic.
Article types and fees
This Research Topic accepts the following article types, unless otherwise specified in the Research Topic description:
Brief Research Report
Case Report
Classification
Clinical Trial
Editorial
FAIR² Data
General Commentary
Hypothesis and Theory
Methods
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Article types
This Research Topic accepts the following article types, unless otherwise specified in the Research Topic description:
Important note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
