Recent Updates on Viral Oncogenesis: Available Preventive and Therapeutic Entities

Abstract

Human viral oncogenesis is a complex phenomenon and a major contributor to the global cancer burden. Several recent findings revealed cellular and molecular pathways that promote the development and initiation of malignancy when viruses cause an infection. Even, antiviral treatment has become an approach to eliminate the viral infections and prevent the activation of oncogenesis. Therefore, for a better understanding, the molecular pathogenesis of various oncogenic viruses like, hepatitis virus, human immunodeficiency viral (HIV), human papillomavirus (HPV), herpes simplex virus (HSV), and Epstein-Barr virus (EBV), could be explored, especially, to expand many potent antivirals that may escalate the apoptosis of infected malignant cells while sparing normal and healthy ones. Moreover, contemporary therapies, such as engineered antibodies antiviral agents targeting signaling pathways and cell biomarkers, could inhibit viral oncogenesis. This review elaborates the recent advancements in both natural and synthetic antivirals to control viral oncogenesis. The study also highlights the challenges and future perspectives of using antivirals in viral oncogenesis.

Estimates of the global burden of non-Hodgkin lymphoma attributable to HIV: a population attributable modeling study

“…According to research, the EBV gp350-Ferritin nanoparticle vaccine (under trials) is expected to reduce the burden of HIV-associated NHL in the future. 58 , 59 …”

Cancer Initiation and Progression: A Comprehensive Review of Carcinogenic Substances, Anti-Cancer Therapies, and Regulatory Frameworks

“…These genetic insults can result in mutations within critical genes, such as proto-oncogenes and tumor suppressor genes. Proto-oncogenes, including RAS, MYC, and EGFR, can undergo activating mutations or amplifications, leading to their constitutive activation and uncontrolled cell proliferation [77]. Conversely, tumor suppressor genes, like TP53, PTEN, and RB1, which normally function as cellular gatekeepers, can be inactivated or lost, compromising their ability to regulate cell cycle progression, DNA repair, and apoptosis [78].…”

Raman Multi-Omic Snapshot and Statistical Validation of Structural Differences between Herpes Simplex Type I and Epstein–Barr Viruses

“…The former subunit, which is the larger of the two, forms a homodimer, meaning two gp350 molecules associate with each other to create a stable complex. On the other hand, the gp220 subunit forms a disulfide-linked heterodimer with gp350, which stabilizes the overall structure of the gp350/220 protein complex [47]. Although the exact structure of gp350/220 has not yet been fully resolved at the atomic level, studies using cryo-electron microscopy and other techniques have provided insights into its overall architecture [48,49].…”