1. ¹Department of Medical Microbiology, MAS University Hospital, Lund University, S-20502 Malmö, Sweden
2. ²Department of Pathology and Clinical Cytology, Sahlgrenska University Hospital, 413 45 Göteborg, Sweden
3. ³Cancer Screening Unit, Oncologic Centre, Karolinska Hospital, 171 76 Stockholm, Sweden
4. ⁴Department of Medical Sciences, Dermatology and Venereology, University Hospital, 751 85 Uppsala, Sweden
5. ⁵Department of Virology, University of Northern Sweden, 901 87 Umeå, Sweden
6. ⁶Institute of Clinical Sciences, Department of Obstetrics and Gynecology, Karolinska Institute, Danderyd Hospital, 182 88 Stockholm, Sweden

Correspondence: Professor J Dillner, E-mail: joakim.dillner@med.lu.se

Revised 11 May 2007; Accepted 16 May 2007; Published online 5 June 2007.

Abstract

We followed a population-based cohort of 5696 women, 32–38 years of age, by registry linkage with cytology and pathology registries during a mean follow-up time of 4.1 years to assess the importance for CIN2+ development of type-specific HPV DNA positivity at baseline. HPV 16, 31 and 33 conveyed the highest risks and were responsible for 33.1, 18.3 and 7.7% of CIN2+ cases, respectively. Women infected with HPV 18, 35, 39, 45, 51, 52, 56, 58, 59 and 66 had significantly lower risks of CIN2+ than women infected with HPV 16. After adjustment for infection with other HPV types, HPV types 35, 45, 59 and 66 had no detectable association with CIN2+. In summary, the different HPV types found in cervical cancer show distinctly different CIN2+ risks, with high risks being restricted to HPV 16 and its close relatives HPV 31 and HPV 33.