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Journal of Clinical Microbiology, February 2008, p. 732-739, Vol. 46, No. 2
0095-1137/08/$08.00+0     doi:10.1128/JCM.01322-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Cervical Human Papillomavirus (HPV) Infection and HPV Type 16 Antibodies in South African Women{triangledown}

Dianne J. Marais,1 Debbie Constant,2 Bruce Allan,1 Henri Carrara,2 Margaret Hoffman,2 Samuel Shapiro,2 Chelsea Morroni,2 and Anna-Lise Williamson1,3*

Institute of Infectious Disease and Molecular Medicine and Division of Medical Virology, Department Clinical Laboratory Sciences, Faculty of Health Sciences, University of Cape Town, Observatory, Cape Town, South Africa,1 School of Public Health and Family Medicine, Faculty of Health Sciences, University of Cape Town, Observatory, Cape Town, South Africa,2 National Health Laboratory Service, Groote Schuur Hospital, Observatory, Cape Town, South Africa3

Received 2 July 2007/ Returned for modification 4 September 2007/ Accepted 28 November 2007

There is a high incidence of cervical cancer in South African women. No large studies to assess human papillomavirus virus (HPV) infection or HPV type 16 (HPV-16) exposure have occurred in the region, a requirement for policy making with regards to HPV screening and the introduction of vaccines. Control women (n = 1,003) enrolled in a case control study of hormonal contraceptives and cervical cancer were tested for 27 cervical HPV types by reverse line blot analysis. The seroprevalence of HPV-16 immunoglobulin G (IgG) and IgA antibodies was assessed by a virus-like particle-based enzyme-linked immunoassay of 908 and 904 control women, respectively, and of 474 women with cervical cancer. The cervical HPV prevalence was 26.1%. The HPV-16 IgG seroprevalence was 44.4% and the HPV-16 IgA seroprevalence was 28.7% in control women, and these levels were significantly higher (61.8% and 52.7%, respectively) for women with cervical cancer (odds ratio [OR], 2.1 and 2.8, respectively). The cervical HPV prevalence showed an association with cervical disease, and the HPV-16 IgG prevalence decreased while the HPV-16 IgA prevalence increased with increasing age (P < 0.05). The prevalence of oncogenic HPV types (including HPV-16) decreased with age, whereas nononcogenic HPV types showed limited association with age. Multivariate analysis revealed cervical HPV infection to be associated with herpes simplex virus type 2 infection (OR, 1.7) and increasing years of education (OR, 1.9). HPV-16 IgG antibodies were inversely associated with current smoking status (OR, 0.6), and the presence of HPV-16 IgA antibodies was inversely associated with the use of alcohol (OR, 2.1) and inversely associated with the use of oral contraceptives (OR, 0.6). High levels of exposure to HPV, and particularly HPV-16, were evident in this population. The apparent increase of serum HPV-16 IgA with increasing age requires further investigation.

* Corresponding author. Mailing address: Institute of Infectious Disease and Molecular Medicine, Faculty of Health Sciences, University of Cape Town, Observatory 7925, Cape Town, Western Cape, South Africa. Phone: 27 21 4066124. Fax: 27 21 4066681. E-mail: anna-lise.williamson{at}uct.ac.za. Address for reprint requests: Institute of Infectious Disease and Molecular Medicine, Faculty of Health Sciences, University of Cape Town, Observatory 7925, Cape Town, Western Cape, South Africa. Phone: 27 21 4066124. Fax: 27 21 4066018. E-mail: di.marais{at}uct.ac.za

{triangledown} Published ahead of print on 12 December 2007.

Journal of Clinical Microbiology, February 2008, p. 732-739, Vol. 46, No. 2
0095-1137/08/$08.00+0     doi:10.1128/JCM.01322-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.





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