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No excess risk of cervical carcinoma among women seropositive for both HPV16 and HPV6/11
Author(s) -
Luostarinen Tapio,
af Geijersstam Veronika,
Bjørge Tone,
Eklund Carina,
Hakama Matti,
Hakulinen Timo,
Jellum Egil,
Koskela Pentti,
Paavonen Jorma,
Pukkala Eero,
Schiller John T.,
Thoresen Steinar,
Youngman Linda D.,
Dillner Joakim,
Lehtinen Matti
Publication year - 1999
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/(sici)1097-0215(19990315)80:6<818::aid-ijc4>3.0.co;2-t
Subject(s) - medicine , cervical cancer , chlamydia trachomatis , oncology , odds ratio , anal carcinoma , hpv infection , carcinoma , gynecology , cancer , immunology , obstetrics , anal cancer
Human papillomavirus (HPV) types 16 and 18 are the major risk factors for cervical carcinoma, whereas HPV types 6 and 11 cause benign genital lesions. We wanted to study the joint effect of simultaneous infections with the oncogenic and non‐oncogenic HPV types on risk of subsequent development of cervical carcinoma. A cohort of 530,000 women who had donated blood samples to Nordic serum banks between 1973 and 1994 was followed up by linkage to national cancer registries. We identified 182 prospective cases with invasive cervical carcinoma and selected 538 matched controls at random. HPV 6, 11, 16, 18 and 33 seropositivity was used as a marker for the different HPV infections, and seropositivity for Chlamydia trachomatis and cotinine were used as markers for risk‐taking sexual behavior and smoking respectively. The adjusted odds ratio (OR) of cervical squamous‐cell carcinoma (SCC) was 2.2 for HPV6/11 among HPV16 seronegatives and 5.5 for HPV16 among HPV6/11 seronegatives. Assuming multiplicative joint effect, the expected OR for seropositivity to both HPV6/11 and HPV16 would have been 12, but the observed OR was 1.0. The antagonistic interaction was statistically significant ( p = 0.001) and present also under deterministic considerations of possible misclassification bias. Antagonistic interactions were also detected for combinations of HPV16 and HPV18 and of HPV16 and HPV33. The results are in line with the concept that HPV‐specific immunity protects against SCC and support primary prevention of SCC by vaccination against the HPVs. Int. J. Cancer 80:818–822, 1999. © 1999 Wiley‐Liss, Inc.