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. 2022 Aug 15;12(8):e971. doi: 10.1002/ctm2.971

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© 2022 The Authors. Clinical and Translational Medicine published by John Wiley & Sons Australia, Ltd on behalf of Shanghai Institute of Clinical Bioinformatics.

This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

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Model of DNA repair pathways involved in the integration of human papillomavirus (HPV), hepatitis B virus (HBV) and Epstein–Barr virus (EBV). Although viruses are replicated in different ways, their common feature is the production of large amounts of double‐stranded linear DNA (dslDNA) and replication forks. When the host cells encounter replication stresses or genetic insults (e.g. ROS), these replication products could serve as substrates of DNA repair pathway for fusion with double stranded DNA breaks (DSBs) generated from human genome, thereby promoting virus integration. Our data demonstrate that viral insertional events of HPV, HBV and EBV are mainly mediated via synthesis‐dependent end‐joining (SD‐EJ) DNA repair mechanism, followed by c‐NHEJ and other alt‐EJ (s‐MMEJ and FoSTeS) DNA repair mechanisms.