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Cancer Causes & Control
Published in: Cancer Causes & Control 12/2014

01-12-2014 | Original paper

Multiple human papillomavirus infection with or without type 16 and risk of cervical intraepithelial neoplasia among women with cervical cytological abnormalities

Authors: Arsenio Spinillo, Barbara Gardella, Marianna Roccio, Paola Alberizzi, Stefania Cesari, Morbini Patrizia, Enrico Silini

Published in: Cancer Causes & Control | Issue 12/2014

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Abstract

Purpose

To evaluate the impact of multiple human papillomavirus (HPV) infections on the risk of cervical intraepithelial neoplasia grade 3 or worse (CIN3+) in subjects with cervical cytological abnormalities.

Methods

A cross-sectional study of 3,842 women attending a colposcopy service was carried out. Genotyping of 18 high-risk, seven low-risk, and two undefined-risk HPVs was carried out by the INNO-LiPA genotyping system.

Results

The final colposcopic/pathological diagnoses were as follows: 1,933 (50.3 %) subjects were negative; 1,041 (27.1 %) CIN1; 280 (7.3 %) CIN2; 520 (13.5 %) CIN3; and 68 (1.8 %) invasive cervical cancer. The prevalence of HPV infection was 75.8 % (2,911/3,842), whereas multiple HPVs were detected in 34.5 % of HPV-positive subjects (2,255/3,842). The adjusted risks of CIN3+ in the group with multiple compared to the group with single infection were 2.31 (95 % CI = 1.54–3.47), among HPV16-positive women, and 3.25 (95 % CI = 2.29–4.61, p = 0.21 compared with HPV16-positive subjects), in HPV16-negative subjects. Out of a total of 1,285 subjects with mild lesions, followed up for a median of 16.1 months (interquartile range = 8.9–36.8), the rate of progression to CIN2–3 was 0.6 % (5/541) among subjects negative or with low-risk HPVs, 1.7 % (8/463) among those with single high-risk HPV, and 5 % (14/281, p < 0.001 compared with HPV-negative/low-risk HPV and p = 0.038 compared with single high-risk HPV) among those with multiple high-risk HPVs.

Conclusions

Among women with cervical cytological abnormalities, infection by multiple high-risk HPVs increased the risk of CIN3+ in both HPV16-positive and HPV16-negative subjects. These findings suggest a potential synergistic interaction between high-risk HPVs, favoring the progression of CIN lesions.
Literature
1.
Cuschieri KS, Cubie HA, Whitley MW et al (2004) Multiple high risk HPV infections are common in cervical neoplasia and young women in a cervical screening population. J Clin Pathol 57:68–72PubMedCentralPubMedCrossRef
2.
Dickson EL, Vogel RI, Bliss RL, Downs LS Jr (2013) Multiple type human papillomavirus (HPV) infections: a cross-sectional analysis of the prevalence of specific types in 309,000 women referred for HPV testing at the time of cervical cytology. Int J Gynecol Cancer 23:1295–1302PubMedCrossRef
3.
Kirschner B, Schledermann D, Holl K et al (2013) HPV-genotypes in high-grade intraepithelial cervical lesions in Danish women. Acta Obstet Gynecol Scand 92:1032–1040PubMedCrossRef
4.
Figueiredo Alves RR, Turchi MD, Santos LE et al (2013) Prevalence, genotype profile and risk factors for multiple human papillomavirus cervical infection in unimmunized female adolescents in Goiânia, Brazil: a community-based study. BMC Public Health 13:1041PubMedCentralPubMedCrossRef
5.
Chaturvedi AK, Katki HA, Hildesheim A et al (2011) Human papillomavirus infection with multiple types: pattern of coinfection and risk of cervical disease. J Infect Dis 203:910–920PubMedCentralPubMedCrossRef
6.
Trottier H, Mahmud S, Costa MC et al (2006) Human papillomavirus infection with multiple types and risk of cervical neoplasia. Cancer Epidemiol Biomark Prev 15:1274–1280CrossRef
7.
De Sanjose S, Quint WGV, Alemany L et al (2010) Human papillomavirus genotype attribution in invasive cervical cancer: a retrospective cross-sectional worldwide study. Lancet Oncol 11:1048–1056PubMedCrossRef
8.
Tota J, Ramanakumar AV, Jiang M et al (2013) Epidemiologic approaches to evaluating the potential for human papillomavirus type replacement postvaccination. Am J Epidemiol 178:625–634PubMedCentralPubMedCrossRef
9.
Mejlhede N, Pedersen BV, Frisch M, Fomsgaard A (2010) Multiple human papilloma virus types in cervical infections: competition or synergy? APMIS 118:346–352PubMedCrossRef
10.
Pista A, de Oliveira CF, Lopes C, Cunha MJ, CLEOPATRE Portugal Study Group (2013) Human papillomavirus type distribution in cervical intraepithelial neoplasia grade 2/3 and cervical cancer in Portugal: a CLEOPATRE II study. Int J Gynecol Cancer 23:500–506PubMedCrossRef
11.
van der Marel J, Quint WGV, Schiffman M et al (2012) Molecular mapping of high grade cervical intraepithelial neoplasia shows etiological dominance of HPV 16. Int J Cancer 131:E946–E953PubMedCentralPubMedCrossRef
12.
Quint W, Jenkins D, Molijn A et al (2012) One virus, one lesion. Individual components of CIN lesions contain a specific HPV type. J Pathol 227:62–71PubMedCrossRef
13.
Bouvard V, Baan R, Straif K et al (2009) A review of human carcinogens—part B. Biological agents. Lancet Oncol 10:321–322PubMedCrossRef
14.
Scott JL, Freese J (2006) Regression models for categorical dependent variables using Stata, 2nd edn. Stata Press, College Station, TX, USA
15.
Massad LS, Einstein MH, Huh WK et al (2013) 2012 updated consensus guidelines for the management of abnormal cervical cancer screening tests and cancer precursors. Obstet Gynecol 121:829–845PubMedCrossRef
16.
Arbyn M, Buntinx F, Van Ranst M, Paraskevaidis E, Martin-Hirsch P, Dillner J (2004) Virologic versus cytologic triage of women with equivocal Pap smears: a meta-analysis of the accuracy to detect high-grade intraepithelial neoplasia. J Natl Cancer Inst 96:280–293PubMedCrossRef
17.
Luostarinen T, af Geijersstam V, Bjørge T et al (1999) No excess risk of cervical carcinoma among women seropositive for both HPV16 and HPV6/11. Int J Cancer 80:818–822PubMedCrossRef
18.
Castle PE, Hunt WC, Langsfeld E, Wheeler CM, New Mexico HPV Pap Registry Steering Committee (2014) Three-year risk of cervical precancer and cancer after the detection of low-risk human papillomavirus genotypes targeted by a commercial test. Obstet Gynecol 123:49–56PubMedCrossRef
19.
Spinillo A, Dal Bello B, Gardella B, Roccio M, Dacco’ MD, Silini EM (2009) Multiple human papillomavirus infection and high grade cervical intraepithelial neoplasia among women with cytological diagnosis of atypical squamous cells of undetermined significance or low grade squamous intraepithelial lesions. Gynecol Oncol 113:115–119PubMedCrossRef
20.
Bayram A, Erkılıç S, Balat Ö et al (2011) Prevalence and genotype distribution of human papillomavirus in non-neoplastic cervical tissue lesion: cervical erosion. J Med Virol 83:1997–2003PubMedCrossRef
21.
Matsumoto K, Oki A, Furuta R et al (2011) Predicting the progression of cervical precursor lesions by human papillomavirus genotyping: a prospective cohort study. Int J Cancer 128:2898–2910PubMedCrossRef
22.
Clarke M, Schiffman M, Wacholder S, Rodriguez AC, Hildesheim A, Quint W, Costa Rican Vaccine Trial Group (2013) A prospective study of absolute risk and determinants of human papillomavirus incidence among young women in Costa Rica. BMC Infect Dis 13:308PubMedCentralPubMedCrossRef
23.
Campos NG, Rodriguez AC, Castle PE et al (2011) Persistence of concurrent infections with multiple human papillomavirus types: a population-based cohort study. J Infect Dis 203:823–827PubMedCentralPubMedCrossRef
24.
Andersson E, Kärrberg C, Rådberg T et al (2012) Type-dependent E6/E7 mRNA expression of single and multiple high-risk human papillomavirus infections in cervical neoplasia. J Clin Virol 54:61–65PubMedCrossRef
25.
An HJ, Sung JM, Park AR et al (2011) Prospective evaluation of longitudinal changes in human papillomavirus genotype and phylogenetic clade associated with cervical disease progression. Gynecol Oncol 120:284–290PubMedCrossRef
Metadata
Title
Multiple human papillomavirus infection with or without type 16 and risk of cervical intraepithelial neoplasia among women with cervical cytological abnormalities
Authors
Arsenio Spinillo
Barbara Gardella
Marianna Roccio
Paola Alberizzi
Stefania Cesari
Morbini Patrizia
Enrico Silini
Publication date
01-12-2014
Publisher
Springer International Publishing
Published in
Cancer Causes & Control / Issue 12/2014
Print ISSN: 0957-5243
Electronic ISSN: 1573-7225
DOI
https://doi.org/10.1007/s10552-014-0471-6

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