© 1995 by Oxford University Press
Journal of the National Cancer Institute, Vol. 87, No. 18, 1365-1371,
September 20, 1995
© 1995 Oxford University Press
Persistent Genital Human Papillomavirus Infection as a Risk Factor for Persistent Cervical Dysplasia
Department of Epidemiology and Social Medicine, Albert Einstein College of Medicine Bronx, NY
Department of Pediatrics, Department of Obstetrics and Gynecology, and Department of Microbiology and Immunology, Albert Einstein College of Medicine Bronx, NY
Department of Obstetrics and Gynecology, Albert Einstein College of Medicine Bronx, NY
Department of Pathology, Albert Einstein College of Medicine Bronx, NY
Department of Epidemiology and Social Medicine, Albert Einstein College of Medicine Bronx, NY
Department of Obstetrics and Gynecology, Albert Einstein College of Medicine Bronx, NY
Department of Obstetrics and Gynecology, Albert Einstein College of Medicine Bronx, NY
Department of Microbiology and Immunology, Albert Einstein College of Medicine Bronx, NY
Department of Microbiology and Immunology, Albert Einstein College of Medicine Bronx, NY
Department of Obstetrics and Gynecology, Albert Einstein College of Medicine Bronx, NY
Correspondence to: Gloria Y. F. Ho, Ph.D., Department of Epidemiology and Social Medicine, Albert Einstein College of Medicine, 1300 Morris Park Ave., Bronx, NY 10461.
Background: Cervical dysplasia, also referred to as squamous intraepithelial lesion (SIL) in cytology or cervical intraepithelial neoplasia in histopathology, is thought to have the potential to advance in progressive stages to cervical cancer. However, not all cases of SIL progress, and most of the mild lesions spontaneously regress. Factors that govern regression, persistence, and progression of SIL are poorly understood. Purpose: Our analysis sought to identify factors that determined persistence or regression of SIL. Methods: Seventy subjects with histopathologically confirmed cervical dysplasia were followed at 3-month intervals for 15 months. At each visit, the cervix was evaluated by Pap smear and colposcopy, and exfoliated cervicovaginal cells were analyzed for human papillomavirus (HPV) DNA. For each subject, data from every two consecutive visits were grouped as a pair. Persistent SIL was considered present if a lesion was detected at a visit (t) as well as at the next visit (t + 1) and absent if a lesion was detected at visit t but not at visit t + 1. A statistical model for time-dependent data correlated persistent SIL with various risk factors. Results: Age, ethnicity, education, sexual behavior, smoking, and the use of oral contraceptives did not correlate with persistent SIL. The risk of persistent SIL was associated with continual HPV infection in visits / and t + 1 (HPV positive by Southern blot analysis: odds ratio [OR] = 3.91, and 95% confidence interval [CI] = 1.58–9.65; HPV positive by polymerase chain reaction [PCR]: OR = 2.42, and 95% CI = 1.03–5.67) and a persistent high viral load (OR = 4.07, and 95% CI = 1.35–12.30). When typed by PCR, individuals with type-specific persistent infection in visits t and t + 1, and particularly those with a continual high viral load (OR = 4.97; 95% CI = 1.45–17.02), had the highest risk for persistent SIL compared with those with a low level of type-specific persistent infection or non-type-specific persistent infection. The presence of persistent HPV infection in visits t – 1 and t (the preceding time interval) was also predictive of persistent SIL in visits t and t + 1, although the strength of association was weaker, suggesting that persistent HPV and SIL occur synchronously. Conclusion: HPV infection and its associated cervical lesions tend to occur concurrently, and type-specific persistent HPV infection, particularly with a high viral load, produces chronic cervical dysplasia. Implications: The natural history of genital HPV infection directly influences the prognosis of cervical dysplasia as measured by persistence of the lesion. Testing for HPV infection may be valuable in the clinical management of women with cervical dysplasia. [J Natl Cancer Inst 1995;87: 1365–71]
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S. Ratnam, E. L. Franco, and A. Ferenczy Human Papillomavirus Testing for Primary Screening of Cervical Cancer Precursors Cancer Epidemiol. Biomarkers Prev., September 1, 2000; 9(9): 945 - 951. [Abstract] [Full Text]
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M.-H. Mayrand, F. Coutlée, C. Hankins, N. Lapointe, P. Forest, M. de Ladurantaye, The Canadian Women's HIV Study Group, and M. Roger Detection of Human Papillomavirus Type 16 DNA in Consecutive Genital Samples Does Not Always Represent Persistent Infection as Determined by Molecular Variant Analysis J. Clin. Microbiol., September 1, 2000; 38(9): 3388 - 3393. [Abstract] [Full Text]
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C. J.L.M. Meijer, P. J.F. Snijders, and A. Brule Screening for cervical cancer: Should we test for infection with high-risk HPV? Can. Med. Assoc. J., September 1, 2000; 163(5): 535 - 538. [Full Text] [PDF]
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L Rozendaal, J Westerga, J C van der Linden, J M M Walboomers, F J Voorhorst, E K J Risse, M E Boon, and C J L M Meijer PCR based high risk HPV testing is superior to neural network based screening for predicting incident CIN III in women with normal cytology and borderline changes J. Clin. Pathol., August 1, 2000; 53(8): 606 - 611. [Abstract] [Full Text] [PDF]
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R. Herrero, A. Hildesheim, C. Bratti, M. E. Sherman, M. Hutchinson, J. Morales, I. Balmaceda, M. D. Greenberg, M. Alfaro, R. D. Burk, et al. Population-Based Study of Human Papillomavirus Infection and Cervical Neoplasia in Rural Costa Rica J Natl Cancer Inst, March 15, 2000; 92(6): 464 - 474. [Abstract] [Full Text] [PDF]
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A M Zaitoun, G McKee, M J Coppen, S M Thomas, and P O G Wilson Completeness of excision and follow up cytology in patients treated with loop excision biopsy J. Clin. Pathol., March 1, 2000; 53(3): 191 - 196. [Abstract] [Full Text] [PDF]
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J. Kónya, G. Veress, A. Juhász, K. Szarka, T. Sápy, Z. Hernádi, and L. Gergely Additional Human Papillomavirus Types Detected by the Hybrid Capture Tube Test among Samples from Women with Cytological and Colposcopical Atypia J. Clin. Microbiol., January 1, 2000; 38(1): 408 - 411. [Abstract] [Full Text]
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R. D. Burk Pernicious Papillomavirus Infection N. Engl. J. Med., November 25, 1999; 341(22): 1687 - 1688. [Full Text]
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K.-L. Liaw, A. G. Glass, M. M. Manos, C. E. Greer, D. R. Scott, M. Sherman, R. D. Burk, R. J. Kurman, S. Wacholder, B. B. Rush, et al. Detection of Human Papillomavirus DNA in Cytologically Normal Women and Subsequent Cervical Squamous Intraepithelial Lesions J Natl Cancer Inst, June 2, 1999; 91(11): 954 - 960. [Abstract] [Full Text] [PDF]
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E. L. Franco, T. E. Rohan, and L. L. Villa Epidemiologic Evidence and Human Papillomavirus Infection as a Necessary Cause of Cervical Cancer J Natl Cancer Inst, March 17, 1999; 91(6): 506 - 511. [Full Text] [PDF]
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J. M. Palefsky, H. Minkoff, L. A. Kalish, A. Levine, H. S. Sacks, P. Garcia, M. Young, S. Melnick, P. Miotti, and R. Burk Cervicovaginal Human Papillomavirus Infection in Human Immunodeficiency Virus-1 (HIV)-Positive and High-Risk HIV-Negative Women J Natl Cancer Inst, February 3, 1999; 91(3): 226 - 236. [Abstract] [Full Text] [PDF]
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J. S. Mandelblatt, P. Kanetsky, L. Eggert, and K. Gold Is HIV Infection a Cofactor for Cervical Squamous Cell Neoplasia? Cancer Epidemiol. Biomarkers Prev., January 1, 1999; 8(1): 97 - 106. [Abstract] [Full Text]
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C. L. Peyton, M. Schiffman, A. T. Lörincz, W. C. Hunt, I. Mielzynska, C. Bratti, S. Eaton, A. Hildesheim, L. A. Morera, A. C. Rodriguez, et al. Comparison of PCR- and Hybrid Capture-Based Human Papillomavirus Detection Systems Using Multiple Cervical Specimen Collection Strategies J. Clin. Microbiol., November 1, 1998; 36(11): 3248 - 3254. [Abstract] [Full Text]
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P. E. Gravitt, C. L. Peyton, R. J. Apple, and C. M. Wheeler Genotyping of 27 Human Papillomavirus Types by Using L1 Consensus PCR Products by a Single-Hybridization, Reverse Line Blot Detection Method J. Clin. Microbiol., October 1, 1998; 36(10): 3020 - 3027. [Abstract] [Full Text]
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P. Zazove, B. D. Reed, L. Gregoire, A. Ferenczy, D. W. Gorenflo, and W. D. Lancaster Low False-Negative Rate of PCR Analysis for Detecting Human Papillomavirus-Related Cervical Lesions J. Clin. Microbiol., September 1, 1998; 36(9): 2708 - 2713. [Abstract] [Full Text]
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S. D. Vernon, E. R. Unger, W. C. Reeves, M. Frisch, H.-O. Adami, M. Melbye, T. V. Ellerbrock, L. Kuhn, and T. C. Wright Human Papillomaviruses and Anogenital Cancer N. Engl. J. Med., March 26, 1998; 338(13): 921 - 922. [Full Text]
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G. Y.F. Ho, R. Bierman, L. Beardsley, C. J. Chang, and R. D. Burk Natural History of Cervicovaginal Papillomavirus Infection in Young Women N. Engl. J. Med., February 12, 1998; 338(7): 423 - 428. [Abstract] [Full Text] [PDF]
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X.-W. Sun, L. Kuhn, T. V. Ellerbrock, M. A. Chiasson, T. J. Bush, and T. C. Wright Human Papillomavirus Infection in Women Infected with the Human Immunodeficiency Virus N. Engl. J. Med., November 6, 1997; 337(19): 1343 - 1349. [Abstract] [Full Text] [PDF]
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