Download Reply to Cervantes To the Editor—The letter from

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
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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
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