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Reply to Cervantes To the Editor—The letter from Dr Cervantes [1] gives us an opportunity to refine the issues and the difficulties encountered when trying to assess risk 1816 d JID 2011:204 (1 December) d CORRESPONDENCE factors for multiple human papillomavirus (HPV) infections. The results from the study of Chaturvedi et al [2] and, more generally, from other studies on the topic [3–6] show that although multiple HPV infections are often found to be more common than would be expected by chance alone, this excess seems to be largely explainable by common risk factors for all HPV infections, rather than by interactions between certain combination of HPV types. Common risk factors for HPV infections, however, are a ‘‘mixed bag’’ and include the sexual behavior of a woman and of her partner(s), as well as biological mechanisms, such as the immune response and the genetic background of the individual. As Cervantes mentioned in his letter, the role of the immunogenetic background of the host in HPV infections is far from clear, although an increasing number of studies are attempting to throw some light on this issue. An increased proportion of multiple HPV infections in immunosuppressed human immunodeficiency virus (HIV)– positive women, compared with HIVnegative women, has been observed [7, 8]. In addition, certain genes involved in DNA repair, viral infection, and cell entry have been found to be associated with important transition steps of cervical carcinogenesis, such as HPV persistence and progression [9]. To the difficulty of characterizing the role of immunogenetic factors as determinants for multiple HPV infections, we must add the usual limitations of epidemiological questionnaires in accurately measuring sexual behavior. In our editorial [10], we emphasized that the use of appropriate statistical models can capture and allow for an overall summary effect of common risk factors for multiple HPV infections. Using such methods, we have observed a 20-fold variation in risk of HPV infection even among women with the same observable risk factors [3]. As yet, however, it has not been possible to quantify the relative contributions of sexual behavior in comparison with biological risk factors. Note Financial support. This work was supported by the Bill & Melinda Gates Foundation (grant 35537). Potential conflicts of interest. All authors: No reported conflicts. All authors have submitted the ICMJE Form for Disclosure of Potential Conflicts of Interest. Conflicts that the editors consider relevant to the content of the manuscript have been disclosed. Salvatore Vaccarella, Martyn Plummer, and Silvia Franceschi International Agency for Research on Cancer, Lyon, France References 1. Cervantes J. Multiple human papillomavirus infection: don’t forget the genetic background. J Infect Dis 2011; 204:1816. 2. Chaturvedi A, Katki H, Hildesheim A, et al. Human papillomavirus infection with multiple types: pattern of co-infection and risk of cervical disease. J Infect Dis 2011; 203:910–20. 3. Plummer M, Schiffman M, Castle PE, MaucortBoulch D, Wheeler CM. A 2-year prospective study of human papillomavirus persistence among women with a cytological diagnosis of atypical squamous cells of undetermined significance or low-grade squamous intraepithelial lesion. J Infect Dis 2007; 195:1582–9. 4. Vaccarella S, Franceschi S, Snijders PJ, Herrero R, Meijer CJ, Plummer M. Concurrent infection with multiple human papillomavirus types: pooled analysis of the IARC HPV Prevalence Surveys. Cancer Epidemiol Biomarkers Prev 2010; 19:503–10. 5. Vaccarella S, Franceschi S, Herrero R, et al. Clustering of multiple human papillomavirus infections in women from a population-based study in Guanacaste, Costa Rica. J Infect Dis 2011; 39:1179–89. 6. Vaccarella S, Plummer M, Franceschi S, et al. Clustering of human papillomavirus (HPV) types in the male genital tract: the HPV in Men (HIM) study. J Infect Dis 2011; doi: 10.1093/infdis/jir595. 7. Chaturvedi AK, Myers L, Hammons AF, et al. Prevalence and clustering patterns of human papillomavirus genotypes in multiple infections. Cancer Epidemiol Biomarkers Prev 2005; 14:2439–45. 8. Banura C, Franceschi S, van Doorn LJ, et al. Infection with human papillomavirus and HIV among young women in Kampala, Uganda. J Infect Dis 2008; 197:555–62. 9. Wang SS, Gonzalez P, Yu K, et al. Common genetic variants and risk for HPV persistence and progression to cervical cancer. PLoS One 2010; 5:e8667. 10. Plummer M, Vaccarella S. Multiple human papillomavirus infections: the exception or the rule? J Infect Dis 2011; 203:891–3. Received 3 August 2011; accepted 4 August 2011; electronically published 10 October 2011. Correspondence: Silvia Franceschi MD, International Agency for Research on Cancer, 150 cours Albert Thomas, 69372 Lyon Cedex 08, France. The Journal of Infectious Diseases 2011;204:1816–7 Ó The Author 2011. Published by Oxford University Press on behalf of the Infectious Diseases Society of America. All rights reserved. For Permissions, please e-mail: journals. [email protected] 1537-6613 (print)/0022-1899 (online)/2011/20411-0024$14.00 DOI: 10.1093/infdis/jir627 CORRESPONDENCE d JID 2011:204 (1 December) d 1817