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REVIEW article

Front. Genet.
Sec. Cancer Genetics and Oncogenomics
Volume 15 - 2024 | doi: 10.3389/fgene.2024.1489324
This article is part of the Research Topic APOBEC and ADAR in Oncogenesis: From Molecular Mechanisms to Therapeutic Targets View all 3 articles

Viral Infection, APOBEC3 Dysregulation, and Cancer

Provisionally accepted
Jake Lehle Jake Lehle Mohadeseh Soleimanpour Moghadam Mohadeseh Soleimanpour Moghadam Samira Mokhtari Samira Mokhtari Diako Ebrahimi Diako Ebrahimi *
  • Texas Biomedical Research Institute, San Antonio, United States

The final, formatted version of the article will be published soon.

    Viral infection plays a significant role in the development and progression of many cancers. Certain viruses, such as Human Papillomavirus (HPV), Epstein-Barr Virus (EBV), and Hepatitis B and C viruses (HBV, HCV), are well-known for their oncogenic potential. These viruses can dysregulate specific molecular and cellular processes through complex interactions with host cellular mechanisms. One such interaction involves a family of DNA mutators known as APOBEC3 (Apolipoprotein B mRNA Editing Catalytic Polypeptide-like 3). The primary function of these cytidine deaminases is to provide protection against viral infections by inducing viral mutagenesis. However, induction and dysregulation of A3 enzymes, driven by viral infection, can inadvertently lead to cellular DNA tumorigenesis. This review focuses on the current knowledge regarding the interplay between viral infection, A3 dysregulation, and cancer, highlighting the molecular mechanisms underlying this relationship.

    Keywords: APOBEC3, viral infection, Cancer, HPV, HBV, ebv, HPyV

    Received: 31 Aug 2024; Accepted: 26 Nov 2024.

    Copyright: © 2024 Lehle, Soleimanpour Moghadam, Mokhtari and Ebrahimi. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    * Correspondence: Diako Ebrahimi, Texas Biomedical Research Institute, San Antonio, United States

    Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.