Human papillomavirus 16 sub-lineage dispersal and cervical cancer risk worldwide: Whole viral genome sequences from 7116 HPV16-positive women.
Adenocarcinoma
/ epidemiology
Carcinoma, Squamous Cell
/ epidemiology
Female
Genetic Variation
Genome, Viral
Genotype
Global Health
High-Throughput Nucleotide Sequencing
Human papillomavirus 16
/ classification
Humans
Papillomavirus Infections
/ complications
Phylogeny
Risk Assessment
Uterine Cervical Neoplasms
/ epidemiology
Whole Genome Sequencing
Cervical cancer
HPV carcinogenesis
HPV epidemiology
HPV genomics
HPV16
Whole virus genome sequencing
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
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
67-74Informations de copyright
Copyright © 2019 International Agency for Research on Cancer. Published by Elsevier B.V. All rights reserved.
Références
J Natl Cancer Inst. 2010 Oct 6;102(19):1478-88
pubmed: 20841605
J Virol. 1997 Mar;71(3):2463-72
pubmed: 9032384
J Clin Microbiol. 1991 Sep;29(9):1765-72
pubmed: 1663516
Int J Gynecol Pathol. 2006 Oct;25(4):393-7
pubmed: 16990718
Cell. 2017 Sep 7;170(6):1164-1174.e6
pubmed: 28886384
J Natl Cancer Inst. 2006 Aug 2;98(15):1045-52
pubmed: 16882941
Int J Cancer. 2000 Jul 15;87(2):221-7
pubmed: 10861478
Int J Cancer. 2017 Aug 15;141(4):664-670
pubmed: 28369882
J Infect Dis. 2007 Jun 1;195(11):1582-9
pubmed: 17471427
J Virol. 2012 Jun;86(12):6855-61
pubmed: 22491459
Int J Cancer. 2005 Apr 10;114(3):422-5
pubmed: 15551313
J Natl Cancer Inst. 2000 Mar 15;92(6):464-74
pubmed: 10716964
Cancer Epidemiol Biomarkers Prev. 2007 Jan;16(1):4-10
pubmed: 17220325
Int J Cancer. 2009 Nov 1;125(9):2151-8
pubmed: 19585494
IARC Monogr Eval Carcinog Risks Hum. 2012;100(Pt B):1-441
pubmed: 23189750
Cancer Res. 2003 Nov 1;63(21):7215-20
pubmed: 14612516
Gynecol Oncol. 2010 May;117(2):297-301
pubmed: 20207397
Bioinformatics. 2012 Oct 1;28(19):2520-2
pubmed: 22908215
Nature. 2017 Mar 16;543(7645):378-384
pubmed: 28112728
Lancet Oncol. 2010 Nov;11(11):1048-56
pubmed: 20952254
Int J Cancer. 2012 Nov 15;131(10):2349-59
pubmed: 22323075
Int J Cancer. 2017 May 1;140(9):2092-2100
pubmed: 28187495
Br J Cancer. 2013 Jan 15;108(1):240-4
pubmed: 23169278
Cancer Epidemiol Biomarkers Prev. 2002 Apr;11(4):343-51
pubmed: 11927494
N Engl J Med. 2003 Feb 6;348(6):518-27
pubmed: 12571259
Lancet. 2013 Sep 7;382(9895):889-99
pubmed: 23618600
Fly (Austin). 2012 Apr-Jun;6(2):80-92
pubmed: 22728672
Papillomavirus Res. 2015 Dec 1;1:3-11
pubmed: 26645052
Lancet. 2005 Sep 17-23;366(9490):991-8
pubmed: 16168781
J Natl Cancer Inst. 2016 Apr 29;108(9):
pubmed: 27130930
Int J Cancer. 2009 Dec 1;125(11):2609-13
pubmed: 19569178
Cancer Med. 2016 Oct;5(10):2909-2919
pubmed: 27654117
J Natl Cancer Inst. 2001 Sep 5;93(17):1325-30
pubmed: 11535707
Virology. 2016 Jan 15;488:156-61
pubmed: 26650690
J Gen Virol. 2000 Dec;81(Pt 12):2959-2968
pubmed: 11086127
Cancer Res. 2010 Apr 15;70(8):3159-69
pubmed: 20354192
PLoS Pathog. 2018 Nov 1;14(11):e1007352
pubmed: 30383862
Mol Biol Evol. 2017 Jan;34(1):4-19
pubmed: 28025273
J Natl Cancer Inst. 1995 Jun 7;87(11):796-802
pubmed: 7791229
Viruses. 2018 Feb 13;10(2):
pubmed: 29438321
J Natl Cancer Inst. 2001 Feb 21;93(4):315-8
pubmed: 11181779
Lancet. 1998 Oct 31;352(9138):1441-2
pubmed: 9807995