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Open Access Highly Accessed Research article

Human papillomavirus (HPV) types 16, 18, 31, 45 DNA loads and HPV-16 integration in persistent and transient infections in young women

Agnihotram V Ramanakumar1, Otelinda Goncalves23, Harriet Richardson1, Pierre Tellier4, Alex Ferenczy5, François Coutlée123 and Eduardo L Franco1*

Author Affiliations

1 Division of Cancer Epidemiology, McGill University, Montreal, Quebec, Canada

2 Laboratoire de Virologie Moléculaire, Centre de Recherche du Centre Hospitalier de l'Université de Montréal, Montreal, Quebec, Canada

3 Département de Microbiologie et Immunologie, Université de Montréal, Montreal, Quebec, Canada

4 Department of Family Medicine, McGill University, Montreal, Quebec, Canada

5 Department of Pathology and Obstetrics & Gynecology, the Sir Mortimer B. Davis-Jewish General Hospital and McGill University, Montreal, Quebec, Canada

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BMC Infectious Diseases 2010, 10:326  doi:10.1186/1471-2334-10-326

Published: 11 November 2010

Abstract

Background

HPV burden is a predictor for high-grade cervical intraepithelial neoplasia and cancer. The natural history of HPV load in young women being recently exposed to HPV is described in this paper.

Methods

A total of 636 female university students were followed for 2 years. Cervical specimens with HPV-16, -18, -31, or -45 DNA by consensus PCR were further evaluated with type-specific and β-globin real-time PCR assays. Proportional hazards regression was used to estimate hazard ratios (HR) of infection clearance. Generalized estimating equations assessed whether HPV loads was predictive of HPV infection at the subsequent visit.

Results

HPV loads were consistently higher among women <25 years old, and those who had multiple sex partners, multiple HPV type infections and smokers. HPV-16 integration was encountered only in one sample. Infection clearance was faster among women at lower tertiles of HPV-16 (HR = 2.8, 95%CI: 1.0-8.1), HPV-18 (HR = 3.5, 95%CI: 1.1-11.2) or combined (HR = 2.4, 95%CI: 1.8-6.2) DNA loads. The relationship between HPV-16 and HPV-18 DNA loads and infection clearance followed a clear dose-response pattern, after adjusting for age and number of sexual partners. GEE Odds Ratios for HPV persistence of the middle and upper tertiles relative to the lower tertile were 2.7 and 3.0 for HPV-16 and 3.8 and 39.1 for HPV-18, respectively. There was no association between HPV-31 or -45 DNA loads and persistence.

Conclusions

The association between HPV load and persistence is not uniform across high-risk genital genotypes. HPV-16 integration was only rarely demonstrated in young women.