Correspondence

HPV Vaccination

N Engl J Med 2009; 361:1610-1611October 15, 2009

Article

To the Editor:

In her review of human papillomavirus (HPV) vaccination (July 16 issue),1 Kahn neglects to discuss one key “area of uncertainty,” namely, the extent to which other high-risk oncogenic HPV types may rapidly occupy the epidemiologic niche vacated by vaccine-targeted HPV types 16 and 18. If this rapid occupation occurs, the large expenditure of health care dollars for widespread HPV vaccination would be rendered futile.

Steven Leiner, N.P.
Mission Neighborhood Health Center, San Francisco, CA
steven.leiner@gmail.com

1 References

1. 1

   Kahn JA. HPV vaccination for the prevention of cervical intraepithelial neoplasia. N Engl J Med 2009;361:271-278
   Full Text | Web of Science | Medline

Author/Editor Response

It is not likely that the prevalence of HPV types not targeted by vaccines will increase to fill an ecologic niche created by a reduction in the prevalence of vaccine-targeted HPVs. First, HPV infections appear to be independent of one another. Several studies have shown that in unvaccinated men and women, preexisting HPV infection does not decrease the probability of being infected by phylogenetically related types.1,2 Thus, HPV genotypes are unlikely to compete with one another for a biologic niche within the epithelium.3 Second, papillomaviruses are DNA viruses that have been stable genetically for millennia, which implies that they will not be able to rapidly mutate and adapt to a new biologic niche.4

Large, population-based surveillance studies that are ongoing will more definitively address the issue of type replacement after vaccination. However, even if these studies show some degree of type replacement, the public health impact is expected to be moderate, given the lower oncogenic risk of the high-risk HPV types not targeted by the vaccines and evidence that vaccination provides some cross-protection against types not targeted by vaccines.5

Jessica A. Kahn, M.D., M.P.H.
Cincinnati Children's Hospital Medical Center, Cincinnati, OH
jessica.kahn@cchmc.org

5 References

1. 1

   Plummer M, Schiffman M, Castle PE, Maucort-Boulch 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;195:1582-1589
   CrossRef | Web of Science | Medline

2. 2

   Kaasila M, Koskela P, Kirnbauer R, Pukkala E, Surcel HM, Lehtinen M. Population dynamics of serologically identified coinfections with human papillomavirus types 11, 16, 18 and 31 in fertile-aged Finnish women. Int J Cancer 2009;125:2166-2172
   CrossRef | Web of Science | Medline

3. 3

   Stanley M, Lowy DR, Frazer I. Prophylactic HPV vaccines: underlying mechanisms. Vaccine 2006;24:Suppl 3:S3/106-S3/113
   Web of Science

4. 4

   Chen Z, DeSalle R, Schiffman M, Herrero R, Burk RD. Evolutionary dynamics of variant genomes of human papillomavirus types 18, 45, and 97. J Virol 2009;83:1443-1455
   CrossRef | Web of Science | Medline

5. 5

   Brown DR, Kjaer SK, Sigurdsson K, et al. The impact of quadrivalent human papillomavirus (HPV: types 6, 11, 16, and 18) L1 virus-like particle vaccine on infection and disease due to oncogenic nonvaccine HPV types in generally HPV-naive women aged 16-26 years. J Infect Dis 2009;199:926-935
   CrossRef | Web of Science | Medline