Human papillomavirus 16 sub-lineage dispersal and cervical cancer risk worldwide: Whole viral genome sequences from 7116 HPV16-positive women.


Journal

Papillomavirus research (Amsterdam, Netherlands)
ISSN: 2405-8521
Titre abrégé: Papillomavirus Res
Pays: Netherlands
ID NLM: 101662552

Informations de publication

Date de publication:
06 2019
Historique:
received: 21 11 2018
accepted: 03 02 2019
pubmed: 10 2 2019
medline: 11 1 2020
entrez: 10 2 2019
Statut: ppublish

Résumé

Human papillomavirus (HPV)16 can be separated into genetic sub-lineages (A1-4, B1-4, C1-4, D1-4) which may have differential cervical cancer risk. A next-generation sequencing assay was used to whole-genome sequence 7116 HPV16-positive cervical samples from well-characterised international epidemiological studies, including 2076 controls, 1878 squamous cell carcinoma (SCC) and 186 adenocarcinoma/adenosquamous cell carcinoma (ADC), and to assign HPV16 sub-lineage. Logistic regression was used to estimate region-stratified country-adjusted odds ratios (OR) and 95%CI. A1 was the most globally widespread sub-lineage, with others showing stronger regional specificity (A3 and A4 for East Asia, B1-4 and C1-4 for Africa, D2 for the Americas, B4, C4 and D4 for North Africa). Increased cancer risks versus A1 were seen for A3, A4 and D (sub)lineages in regions where they were common: A3 in East Asia (OR=2.2, 95%CI:1.0-4.7); A4 in East Asia (6.6, 3.1-14.1) and North America (3.8, 1.7-8.3); and D in North (6.2, 4.1-9.3) and South/Central America (2.2, 0.8-5.7), where D lineages were also more frequent in ADC than SCC (3.2, 1.5-6.5; 12.1, 5.7-25.6, respectively). HPV16 genetic variation can strongly influence cervical cancer risk. However, burden of cervical cancer attributable to different sub-lineages worldwide is largely driven by historical HPV16 sub-lineage dispersal.

Sections du résumé

BACKGROUND
Human papillomavirus (HPV)16 can be separated into genetic sub-lineages (A1-4, B1-4, C1-4, D1-4) which may have differential cervical cancer risk.
METHODS
A next-generation sequencing assay was used to whole-genome sequence 7116 HPV16-positive cervical samples from well-characterised international epidemiological studies, including 2076 controls, 1878 squamous cell carcinoma (SCC) and 186 adenocarcinoma/adenosquamous cell carcinoma (ADC), and to assign HPV16 sub-lineage. Logistic regression was used to estimate region-stratified country-adjusted odds ratios (OR) and 95%CI.
RESULTS
A1 was the most globally widespread sub-lineage, with others showing stronger regional specificity (A3 and A4 for East Asia, B1-4 and C1-4 for Africa, D2 for the Americas, B4, C4 and D4 for North Africa). Increased cancer risks versus A1 were seen for A3, A4 and D (sub)lineages in regions where they were common: A3 in East Asia (OR=2.2, 95%CI:1.0-4.7); A4 in East Asia (6.6, 3.1-14.1) and North America (3.8, 1.7-8.3); and D in North (6.2, 4.1-9.3) and South/Central America (2.2, 0.8-5.7), where D lineages were also more frequent in ADC than SCC (3.2, 1.5-6.5; 12.1, 5.7-25.6, respectively).
CONCLUSIONS
HPV16 genetic variation can strongly influence cervical cancer risk. However, burden of cervical cancer attributable to different sub-lineages worldwide is largely driven by historical HPV16 sub-lineage dispersal.

Identifiants

pubmed: 30738204
pii: S2405-8521(18)30137-X
doi: 10.1016/j.pvr.2019.02.001
pmc: PMC6374642
pii:
doi:

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

67-74

Informations de copyright

Copyright © 2019 International Agency for Research on Cancer. Published by Elsevier B.V. All rights reserved.

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Auteurs

Gary M Clifford (GM)

International Agency for Research on Cancer, Lyon, France. Electronic address: CliffordG@iarc.fr.

Vanessa Tenet (V)

International Agency for Research on Cancer, Lyon, France. Electronic address: TenetV@iarc.fr.

Damien Georges (D)

International Agency for Research on Cancer, Lyon, France. Electronic address: GeorgesD@iarc.fr.

Laia Alemany (L)

Infections and Cancer Unit, Cancer Epidemiology Research Program, Catalan Institute of Oncology, Bellvitge Institute of Biomedical Research, Barcelona, Spain; CIBER en Epidemiología y Salud Pública (CIBERESP), Barcelona, Spain. Electronic address: lalemany@iconcologia.net.

Miquel Angel Pavón (MA)

Infections and Cancer Unit, Cancer Epidemiology Research Program, Catalan Institute of Oncology, Bellvitge Institute of Biomedical Research, Barcelona, Spain; CIBER en Oncología (CIBERONC), Barcelona, Spain. Electronic address: mpavon@iconcologia.net.

Zigui Chen (Z)

Department of Microbiology, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong SAR, China. Electronic address: zigui.chen@cuhk.edu.hk.

Meredith Yeager (M)

Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Rockville, MD, USA; Cancer Genomics Research Laboratory, Leidos Biomedical Research, Inc., Frederick, MD, USA. Electronic address: yeagerm@mail.nih.gov.

Michael Cullen (M)

Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Rockville, MD, USA; Cancer Genomics Research Laboratory, Leidos Biomedical Research, Inc., Frederick, MD, USA. Electronic address: michael.cullen@nih.gov.

Joseph F Boland (JF)

Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Rockville, MD, USA; Cancer Genomics Research Laboratory, Leidos Biomedical Research, Inc., Frederick, MD, USA. Electronic address: bolandj2@mail.nih.gov.

Sara Bass (S)

Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Rockville, MD, USA; Cancer Genomics Research Laboratory, Leidos Biomedical Research, Inc., Frederick, MD, USA. Electronic address: sara.bass2@nih.gov.

Mia Steinberg (M)

Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Rockville, MD, USA; Cancer Genomics Research Laboratory, Leidos Biomedical Research, Inc., Frederick, MD, USA. Electronic address: mia.steinberg@nih.gov.

Tina Raine-Bennett (T)

Women's Health Research Institute, Division of Research, Kaiser Permanente Northern California, Oakland, CA, USA. Electronic address: Tina.R.Raine-Bennett@kp.org.

Thomas Lorey (T)

Regional Laboratory, Kaiser Permanente Northern California, Oakland, CA, USA. Electronic address: thomas.lorey@kp.org.

Nicolas Wentzensen (N)

Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Rockville, MD, USA. Electronic address: wentzenn@mail.nih.gov.

Joan Walker (J)

University of Oklahoma Health Sciences Center, Oklahoma City, USA. Electronic address: joan-walker@ouhsc.edu.

Rosemary Zuna (R)

University of Oklahoma Health Sciences Center, Oklahoma City, USA. Electronic address: rosemary-zuna@ouhsc.edu.

Mark Schiffman (M)

Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Rockville, MD, USA. Electronic address: schiffmm@exchange.nih.gov.

Lisa Mirabello (L)

Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Rockville, MD, USA. Electronic address: mirabellol@mail.nih.gov.

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