Natural History of HPV Infections

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Applied Evidence

Natural History of HPV Infections

J Fam Pract. 2009 September;58(9):S3-S7

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References

1. Burchell AN, Winer RL, de Sanjose S, et al. Chapter 6: Epidemiology and transmission dynamics of genital HPV infection. Vaccine. 2006;24 (suppl 3):S52-S61.

2. Winer RL, Hughes JP, Feng Q, et al. Condom use and the risk of genital human papillomavirus infection in young women. N Engl J Med. 2006;354:2645-2654.

3. Winer RL, Lee SK, Hughes JP, et al. Genital human papillomavirus infection: incidence and risk factors in a cohort of female university students. Am J Epidemiol. 2003;157:218-226.

4. Castellsague X, Drudis T, Canadas MP, et al. Human papillomavirus (HPV) infection in pregnant women and mother-to-child transmission of genital HPV genotypes: a prospective study in Spain. BMC Infect Dis. 2009;9:74.

5. Brown DR, Shew ML, Qadadri B, et al. A longitudinal study of genital human papillomavirus infection in a cohort of closely followed adolescent women. J Infect Dis. 2005;191:182-192.

6. Richardson H, Kelsall G, Tellier P, et al. The natural history of type-specific human papillomavirus infections in female university students. Cancer Epidemiol Biomarkers Prev. 2003;12:485-490.

7. Ho GY, Bierman R, Beardsley L, et al. Natural history of cervicovaginal papillomavirus infection in young women. N Engl J Med. 1998;338:423-428.

8. Schiffman M, Castle PE, Jeronimo J, et al. Human papillomavirus and cervical cancer. Lancet. 2007;370:890-907.

9. Castle PE, Wacholder S, Sherman ME, et al. Absolute risk of a subsequent abnormal pap among oncogenic human papillomavirus DNA-positive, cytologically negative women. Cancer. 2002;95:2145-2151.

10. Moscicki AB, Shiboski S, Hills NK, et al. Regression of low-grade squamous intra-epithelial lesions in young women. Lancet. 2004;364:1678-1683.

11. Castle PE, Fetterman B, Poitras N, et al. Five-year experience of human papillomavirus DNA and Papanicolaou test cotesting. Obstet Gynecol. 2009;113:595-600.

12. Wright TC, Kuhn L. Immunosuppression and the cervix; human immunodeficiency virus (HIV). In: Jordan JA, Singer A, eds. The Cervix. Malden, MA: Blackwell; 2006:450–517.

13. Sawaya GF, McConnell KJ, Kulasingam SL, et al. Risk of cervical cancer associated with extending the interval between cervical-cancer screenings. N Engl J Med. 2003;349:1501-1509.

14. Winer RL, Kiviat NB, Hughes JP, et al. Development and duration of human papillomavirus lesions, after initial infection. J Infect Dis. 2005;191:731-738.

15. Mao C, Koutsky LA, Ault KA, et al. Efficacy of human papillomavirus-16 vaccine to prevent cervical intraepithelial neoplasia: a randomized controlled trial. Obstet Gynecol. 2006;107:18-27.

16. Kjaer S, Hogdall E, Frederiksen K, et al. The absolute risk of cervical abnormalities in high-risk human papillomavirus-positive, cytologically normal women over a 10-year period. Cancer Res. 2006;66:10630-10636.

17. Naucler P, Ryd W, Tornberg S, et al. HPV type-specific risks of high-grade CIN during 4 years of follow-up: a population-based prospective study. Br J Cancer. 2007;97:129-132.

18. Khan MJ, Castle PE, Lorincz AT, et al. The elevated 10-year risk of cervical precancer and cancer in women with human papillomavirus (HPV) type 16 or 18 and the possible utility of type-specific HPV testing in clinical practice. J Natl Cancer Inst. 2005;97:1072-1079.

FIGURE 2
Cumulative detection of CIN 2,3 after incident HPV infections in two studies

HPV, human papillomavirus.
After incident HPV 16 infection (green line) and after incident HPV 16 or 18 infection (blue line).
Modified from Winer RL, et al. J Infect Dis. 2005;191:731-738 (blue line); Mao C, et al. Obstet Gynecol. 2006;107:18-27 (green line).

TABLE
Detection of CIN 2,3 or cancer

HPV status	Percent with CIN 2+*
HPV negative	0.4%
HPV 16	37%
HPV 18	26%
HPV 31	37%
HPV 33	48%
HPV 52	26%
HPV 58	30%
CIN, cervical intraepithelial neoplasia; HPV, human papillomavirus.
*Percentage of women diagnosed with CIN 2,3 or cancer during a 4-year follow-up period.
Modified from Naucler P, et al. Br J Cancer. 2007;97:129-132.

TAKE-HOME POINTS

HPV infections are common, and approximately half of young women become infected within 4 years of initiating sexual activity.
The predominant mode of transmission of HPV is by sexual intercourse; consistent use of condoms reduces, but does not prevent, transmission.
More than 80% of HPV infections spontaneously clear over a 3-year period.
Less than 5% of women in the general population are high-risk HPV positive by the age of 45 years.
HPV 16 and HPV 18 are quite oncogenic, and about 1 out of 4 infected individuals will develop CIN 2,3 over a 3-year period.