ArticleTumour virus research2022
Differences in integration frequencies and APOBEC3 profiles of five high-risk HPV types adheres to phylogeny.
Article in Tumour virus research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- HPV genotype distribution and cervical lesions in colposcopy-referred women in Western China: a cross-sectional study.BMC cancer · 2026Article
- Drug Repositioning for HPV Clade-Specific Cervicouterine Cancer Using the OCTAD Pipeline.International journal of molecular sciences · 2025Article
- From Viral Infection to Genome Reshaping: The Triggering Role of HPV Integration in Cervical Cancer.International journal of molecular sciences · 2025Review
- Genotype distribution and molecular characterization of HPV in the Peruvian amazon: insights into prevalence, lineage diversity, and viral integration.Scientific reports · 2025Article
- Human papillomavirus genomes associate with active host chromatin during persistent viral infection.PLoS pathogens · 2025Article
- Viral infection, APOBEC3 dysregulation, and cancer.Frontiers in genetics · 2024Review
- Intra-Patient Genomic Variations of Human Papillomavirus Type 31 in Cervical Cancer and Precancer.Viruses · 2023Article
- TaME-seq2: tagmentation-assisted multiplex PCR enrichment sequencing for viral genomic profiling.Virology journal · 2023Article
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Persistent infection with Human Papillomavirus (HPV) is responsible for almost all cases of cervical cancers, and HPV16 and HPV18 associated with the majority of these. These types differ in the proportion of viral minor nucleotide variants (MNVs) caused by APOBEC3 mutagenesis as well as integration frequencies. Whether these traits extend to other types remains uncertain. This study aimed to investigate and compare genomic variability and chromosomal integration in the two phylogenetically distinct Alpha-7 and Alpha-9 clades of carcinogenic HPV types. The TaME-seq protocol was employed to sequence cervical cell samples positive for HPV31, HPV33 or HPV45 and combine these with data from a previous study on HPV16 and HPV18. APOBEC3 mutation signatures were found in Alpha-9 (HPV16/31/33) but not in Alpha-7 (HPV18/45). HPV45 had significantly more MNVs compared to the other types. Alpha-7 had higher integration frequency compared to Alpha-9. An increase in integration frequency with increased diagnostic severity was found for Alpha-7. The results highlight important differences and broaden our understanding of the molecular mechanisms behind cervical cancer induced by high-risk HPV types from the Alpha-7 and Alpha-9 clades.
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