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. 2022 May 10;13:2563. doi: 10.1038/s41467-022-30190-1

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© The Author(s) 2022

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 1 — a Distribution of integration breakpoints across human and virus genomes. The colored link line indicates which human chromosome and which virus gene the integration breakpoint had occurred on. Only HPV16-related breakpoints are shown. b Comparison of the observed and expected numbers of breakpoints in the viral genome. The expected number of breakpoints was calculated based on the assumption that breakpoints are uniformly distributed across the viral genome. Only HPV16-related breakpoints are shown (n = 61). P values were calculated by a two-sided binomial test. c Integration breakpoints are often clustered within the same sample in the human genome. Dots represent integration breakpoints and color keys indicate sample sources. Source data are provided as a Source Data file.