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Chronic disease
P2-164 Human papillomavirus, other sexually transmitted infections and risk of cervical cancer. A Nordic Joint Study
  1. T Luostarinen1,
  2. L A Dahlström2,
  3. K Andersson3,
  4. H Ögmundsdottir4,
  5. E Jellum5,
  6. P Koskela6,
  7. G Wadell7,
  8. M Lehtinen8,
  9. J Dillner3,9
  1. 1Finnish Cancer Registry, Helsinki, Finland
  2. 2MEB, Karolinska Institutet, Stockholm, Sweden
  3. 3Department of Laboratory Medicine, Medical Microbiology, Lund University, Malmö, Sweden
  4. 4Cancer Research Laboratory, Faculty of Medicine, University of Iceland, Reykjavik, Iceland
  5. 5Institute of Clinical Biochemistry, Oslo University Hospital, Rikshospitalet, Oslo, Norway
  6. 6National Institute for Health and Welfare, Oulu, Finland
  7. 7Department of Clinical Microbiology, Virology, Umeå University, Umeå, Sweden
  8. 8University of Tampere, Tampere, Finland
  9. 9Department of Laboratory Medicine, Karolinska Institutet, Stockholm, Sweden

Abstract

Introduction Human papillomavirus (HPV) is considered necessary cause of invasive cervical cancer (ICC), but relations between different HPV types and other sexually transmitted infections in cervical carcinogenesis are unresolved. The CCRPB-EU Network conducted a large study, aiming to assess how major high- and low-risk HPV types, 16, 18 and 6, and possible cofactors, Chlamydia trachomatis and herpes simplex virus type 2 (HSV-2), interact in the aetiology of cervical cancer.

Methods A case-control study was nested in four Nordic serum banks containing serum samples from approximately 1 000 000 women. Linkage to cancer registries resulted to 604 ICC cases diagnosed after serum sampling. Five controls were matched to bank, age at sampling and storage time. IgG antibodies specific for HPV types, C trachomatis and HSV-2 were determined, and tobacco smoke exposure measured by serum cotinine, and HPV DNA in cancer tissue PCR-tested. ORs were estimated by conditional logistic regression, and adjusted for cotinine and for HPV16, HPV18 and C trachomatis, when applicable.

Results Seropositivity for HPV16 did not confer any increased risk for HPV18 DNA positive cancer and HPV18 seropositivity had no association with HPV16 DNA positive cancer. HPV6 had no effect on its own but an antagonistic joint effect with HPV16. HSV-2 had little or no association. C trachomatis had a strongly increased risk for cervical cancer, which remained also among HPV18 seropositives.

Conclusions Type-specific HPV DNA persistence is important in cervical carcinogenesis. HSV-2 is possibly not a cofactor, but C trachomatis is probably a strong cofactor for ICC.

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