© The Author 2007. Published by Oxford University Press.
CORRESPONDENCE |
Re: Human Papillomavirus Type 16 and 18 Variants: Race-Related Distribution and Persistence
Affiliations of authors: Department of Virology, Ludwig Institute for Cancer Research, São Paulo, Brazil (LS, SF, LLV); Department of Biochemistry, Chemistry Institute, University of São Paulo, São Paulo, Brazil (LS); Division of Cancer Epidemiology (HT, ELF) and Department of Family Medicine (EDF), McGill University, Montreal, Canada
Correspondence to: Luisa Lina Villa, Ludwig Institute for Cancer Research, R Prof Antonio Prudente 109, 4th Floor, 01509-010 São Paulo, SP, Brazil (e-mail: llvilla{at}ludwig.org.br).
Non-European variants of human papillomaviruses (HPVs) 16 and 18 are associated with increased risk of developing preinvasive cervical lesions (1). In a recent article in this Journal, Xi et al. (2) showed that European and African variants of HPVs 16 and 18 were predominantly detected in white and African American women, respectively. Most importantly, they showed that infections with these variants tend to persist longer in women whose ancestry matches that of the variant's geographic origin. Race was self-reported by study participants.
Prompted by these compelling findings, we used Kaplan–Meier analysis and log-rank tests to assess the outcomes of prevalent and incident variant-specific infection with HPVs 16 and/or 18 by different racial categories among women from the Ludwig/McGill cohort study conducted in Brazil (3). The subject's race was inferred by trained nurses during an interview. Race categories were combined for analysis as white and nonwhite, with the latter category being composed mostly of black women or women with visible African–Brazilian ancestry. European variants of HPVs 16 or 18 were detected in 166 women who were followed for a period of 5 years, as previously described (1). White women had 78 (60%) of the 130 infections with European HPVs 16 and 21 (65%) of the 32 infections with European HPV 18. In addition, one white and three nonwhite women were positive for European variants of both HPV types. Prevalent and incident HPVs 16 and 18 infections cleared at comparable rates between white and nonwhite women who were infected with European variants of these two types (P = .436, Fig. 1). Comparable distributions of clearance times were observed for prevalent and incident infections with HPVs 16 or 18 that were analyzed independently and compared European and non-European variants in the two racial categories described above.
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Our results are, however, more in line with those of Hildesheim et al. (4) who did not observe any ethnic difference between individuals with European HPV16 variants in a study conducted in Costa Rica. In that study, microsatellite markers were analyzed to determine the degree of genetic relatedness among individuals. The lack of an association between persistence of a given variant and the racial ancestry of the host in our study and in that of Hildesheim et al. may have originated from the greater racial admixing in the two Latin American populations studied compared with that in the US population. At least for the Brazilian population, it has been shown that the physical appearance of an individual is a poor predictor of genomic African ancestry (5). In the study of Xi et al., the analysis was limited to white and African American women, which are two visibly distinct ethnic groups in the United States.
Xi et al. provided evidence for an evolutionary process that resulted in greater adaptability of certain intratypic variants to specific human population groups. This process likely results from a complex interplay between multiple genetic polymorphisms in HPV and its human host, some of which may mediate mechanisms of susceptibility and immune evasion. Unfortunately, racial admixing in Brazil and in other Latin American countries may not permit ready corroboration of this phenomenon.
REFERENCES
(1) Sichero L, Ferreira S, Trottier H, Duarte-Franco E, Ferenczy A, Franco EL. High grade cervical lesions are caused preferentially by non-European variants of HPVs 16 and 18. Int J Cancer. In press 2006.
(2) Xi LF, Kiviat NB, Hildesheim A, Galloway DA, Wheeler CM, Ho J. Human papillomavirus type 16 and 18 variants: race related distribution and persistence. J Natl Cancer Inst (2006) 98:1045–52.
(3) Franco E, Villa L, Rohan T, Ferenczy A, Petzl-Erler M, Matlashewski G. Design and methods of the Ludwig-McGill longitudinal study of the natural history of human papillomavirus infection and cervical neoplasia in Brazil. Ludwig-McGill Study Group. Rev Panam Salud Publica (1999) 6:223–33.[Medline]
(4) Hildesheim A, Schiffman M, Bromley C, Wacholder S, Herrero R, Rodriguez A. Human papillomavirus type 16 variants and risk of cervical cancer. J Natl Cancer Inst (2001) 93:315–8.
(5) Parra FC, Amado RC, Lambertucci JR, Rocha J, Antunes CM, Pena SJD. Color and genomic ancestry in Brazilians. Proc Natl Acad Sci U S A (2003) 100:177–82.
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J Natl Cancer Inst 2006 98: 1045-1052.
J Natl Cancer Inst 2007 99: 654-655.
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