Molecular Mechanisms of Viral Oncogenesis in Humans

The document from August 24, 2018, reviews the molecular mechanisms by which seven oncogenic viruses—Epstein-Barr virus (EBV), hepatitis B virus (HBV), human T-lymphotropic virus 1 (HTLV-1), human papillomaviruses (HPVs), hepatitis C virus (HCV), Kaposi sarcoma-associated herpesvirus (KSHV), and Merkel cell polyomavirus (MCPyV)—contribute to approximately 15-20% of all human cancers. These viruses manipulate host cell signaling, DNA damage responses, immunity, and microRNA targets to promote cancer, often by encoding oncoproteins that dysregulate tumor suppressor pathways like p53 and retinoblastoma protein (pRB). The review details how these viruses target various signaling pathways, including MAPK, PI3K-AKT, Notch, WNT/β-catenin, and NF-κB, to enhance viral assembly and promote cell proliferation and survival. It also discusses how viruses engage the DNA damage response to optimize the cellular environment for replication, leading to genomic instability and cancer progression. Furthermore, the document describes how viruses evade immune detection and manipulate immune responses, which can lead to malignancies, especially in immunocompromised individuals. Finally, it highlights the effectiveness of antiviral therapies and vaccinations in reducing the incidence of viral cancers and suggests that targeted chemotherapies and immunotherapies specific to viral oncogenic mechanisms could lead to better clinical outcomes. Advances in omics technologies are expected to further the understanding of virus-host interactions and improve intervention strategies for viral-induced cancers.