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Animal: DNA Viruses |
vall- Lundqvist2
Microbiology and Tumor Biology Center, Karolinska Institute, Box 280, S-171 77 Stockholm, Sweden1
Department of Gynaecologic Oncology, Radiumhemmet, Karolinska Hospital, Stockholm, Sweden2
University of Latvia, Riga, Latvia3
Department of Medical Microbiology, University of Mainz, Mainz, Germany4
Laboratory of Cellular Oncology, The National Cancer Institute, Bethesda, MD, USA5
Department of Infectious Disease Epidemiology, National Public Health Institute, Helsinki, Finland6
Author for correspondence: Joakim Dillner (at the Karolinska Institute). Fax +46 8 326 702. e-mail joakim.dillner{at}mtc.ki.se
Human papillomavirus (HPV) exists as more than 100 genotypes. It is not well-established whether the different HPV types interfere with infection or pathogenesis by each other. Possible interactions in cervical carcinogenesis between infection with the most common HPV types (6, 11, 16, 18 and 33) were studied in a seroepidemiological case- control study of 218 women with primary untreated cervical cancer and 219 healthy age-matched control women. As previously shown, HPV-16 seropositivity was associated with cervical cancer risk [odds ratio (OR), 2·39], but HPV-16 was not associated with cervical cancer risk among HPV-6 seropositive women (OR, 1·0). The relative excess risk due to interaction between HPV-6 and -16 was -2·35 (95% confidence interval, -0·04 to -4·65), indicating significant antagonism. The results suggest that infection with HPV-6 may interfere with HPV-16-associated cervical carcinogenesis.
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