HPV16 and HPV18 type-specific APOBEC3 and integration profiles in different diagnostic categories of cervical samples.

Autor:	Lagström S; Department of Microbiology and Infection Control, Akershus University Hospital, Lørenskog, Norway; Department of Research, Cancer Registry of Norway, Oslo, Norway; Institute of Clinical Medicine, University of Oslo, Oslo, Norway., Løvestad AH; Faculty of Health Sciences, OsloMet, Oslo Metropolitan University, Oslo, Norway., Umu SU; Department of Research, Cancer Registry of Norway, Oslo, Norway., Ambur OH; Faculty of Health Sciences, OsloMet, Oslo Metropolitan University, Oslo, Norway., Nygård M; Department of Research, Cancer Registry of Norway, Oslo, Norway., Rounge TB; Department of Research, Cancer Registry of Norway, Oslo, Norway; Department of Informatics, University of Oslo, Oslo, Norway. Electronic address: trine.rounge@kreftregisteret.no., Christiansen IK; Department of Microbiology and Infection Control, Akershus University Hospital, Lørenskog, Norway; Department of Clinical Molecular Biology (EpiGen), Division of Medicine, Akershus University Hospital and University of Oslo, Lørenskog, Norway. Electronic address: irene.kraus.christiansen@ahus.no.
Jazyk:	angličtina
Zdroj:	Tumour virus research [Tumour Virus Res] 2021 Dec; Vol. 12, pp. 200221. Date of Electronic Publication: 2021 Jun 25.
DOI:	10.1016/j.tvr.2021.200221
Abstrakt:	Human papillomavirus (HPV) 16 and 18 are the most predominant types in cervical cancer. Only a small fraction of HPV infections progress to cancer, indicating that additional factors and genomic events contribute to the carcinogenesis, such as minor nucleotide variation caused by APOBEC3 and chromosomal integration. We analysed intra-host minor nucleotide variants (MNVs) and integration in HPV16 and HPV18 positive cervical samples with different morphology. Samples were sequenced using an HPV whole genome sequencing protocol TaME-seq. A total of 80 HPV16 and 51 HPV18 positive samples passed the sequencing depth criteria of 300× reads, showing the following distribution: non-progressive disease (HPV16 n = 21, HPV18 n = 12); cervical intraepithelial neoplasia (CIN) grade 2 (HPV16 n = 27, HPV18 n = 9); CIN3/adenocarcinoma in situ (AIS) (HPV16 n = 27, HPV18 n = 30); cervical cancer (HPV16 n = 5). Similar numbers of MNVs in HPV16 and HPV18 samples were observed for most viral genes, with the exception of HPV18 E4 with higher numbers across clinical categories. APOBEC3 signatures were observed in HPV16 lesions, while similar mutation patterns were not detected for HPV18. The proportion of samples with integration was 13% for HPV16 and 59% for HPV18 positive samples, with a noticeable portion located within or close to cancer-related genes. (Copyright © 2021 The Author(s). Published by Elsevier B.V. All rights reserved.)
Databáze:	MEDLINE
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