ArticlePLoS pathogens2020
High-resolution analysis of Merkel Cell Polyomavirus in Merkel Cell Carcinoma reveals distinct integration patterns and suggests NHEJ and MMBIR as underlying mechanisms.
Article in PLoS pathogens, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 38 citations in OpenAlex.
- The Significance of cGAS-STING Signaling in Response to Oncogenic Viruses.Cell biochemistry and function · 2026Review
- Antiviral regulator TRIM25 as a prognostic marker of better survival in Merkel cell carcinoma: Association with MCPyV status.International journal of cancer · 2026Article
- A Lab-on-a-Chip for the Extraction and Analysis of Single Molecules of DNA from Biological Media.Nanomaterials (Basel, Switzerland) · 2026Article
- Classification, functions, evolution, and applications of defective viral genomes.Frontiers in microbiology · 2026Review
- Interlocking host and viral cis-regulatory networks drive Merkel cell carcinoma.The Journal of clinical investigation · 2025Article
- Molecular dynamics simulation-driven focused virtual screening and experimental validation of Fisetin as an inhibitor of Helicobacter pylori HtrA protease.Molecular diversity · 2025Article
- Merkel cell carcinoma of the parotid gland: a rare case report and literature review.International journal of surgery case reports · 2025Article
- Genomic Signatures of Poor Prognosis in Merkel Cell Carcinoma: A Single-Institution Prospective Study.Molecular cancer research : MCR · 2025Article
- Genome integration of human DNA oncoviruses.Journal of virology · 2025Review
- Review
- Review
- Defective but tumorigenic: the evolutionary and functional roles of mutated oncoviruses.FEMS microbiology reviews · 2025Review
- The pathogen's playbook in cancer: from oncogenesis to progression.Frontiers in oncology · 2025Review
- Intra-host genomic diversity and integration landscape of human tissue-resident DNA virome.Nucleic acids research · 2024Article
- Review
- Microhomology-mediated repair machinery and its relationship with HPV-mediated oncogenesis.Journal of medical virology · 2024Review
- For Better or Worse: Modulation of the Host DNA Damage Response by Human Papillomavirus.Annual review of virology · 2023Review
- Evidence for virus-mediated oncogenesis in bladder cancers arising in solid organ transplant recipients.eLife · 2023Article
- Immunogenic Properties and Antigenic Similarity of Virus-like Particles Derived from Human Polyomaviruses.International journal of molecular sciences · 2023Article
- Merkel Cell Polyomavirus: Infection, Genome, Transcripts and Its Role in Development of Merkel Cell Carcinoma.Cancers · 2023Review
Corrections and comments
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Authors and funding
15 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Merkel Cell Polyomavirus (MCPyV) is the etiological agent of the majority of Merkel Cell Carcinomas (MCC). MCPyV positive MCCs harbor integrated, defective viral genomes that constitutively express viral oncogenes. Which molecular mechanisms promote viral integration, if distinct integration patterns exist, and if integration occurs preferentially at loci with specific chromatin states is unknown. We here combined short and long-read (nanopore) next-generation sequencing and present the first high-resolution analysis of integration site structure in MCC cell lines as well as primary tumor material. We find two main types of integration site structure: Linear patterns with chromosomal breakpoints that map closely together, and complex integration loci that exhibit local amplification of genomic sequences flanking the viral DNA. Sequence analysis suggests that linear patterns are produced during viral replication by integration of defective/linear genomes into host DNA double strand breaks via non-homologous end joining, NHEJ. In contrast, our data strongly suggest that complex integration patterns are mediated by microhomology-mediated break-induced replication, MMBIR. Furthermore, we show by ChIP-Seq and RNA-Seq analysis that MCPyV preferably integrates in open chromatin and provide evidence that viral oncogene expression is driven by the viral promoter region, rather than transcription from juxtaposed host promoters. Taken together, our data explain the characteristics of MCPyV integration and may also provide a model for integration of other oncogenic DNA viruses such as papillomaviruses.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.