[Epidemiology of cervical papillomavirus infections. Recent knowledge].
GENERAL DATA: There is now considerable evidence that high risk human papillomaviruses (HPV), such as HPV 16, are closely associated with cancer of the cervix. HPVs that are primarily transmitted through sexual contact, are found in over 99% of the cases of invasive cervical cancer. Although most women can be infected during their sexual life, a small minority is at risk for developing cancer. The long latency period between primary infection and cancer emergence suggests that additional factors are involved in the process of tumor development: sexual behavior, immune status, genetic predispositions, nutritional status, tobacco use, socio-economical level. NATURAL HISTORY: HPVs infect epithelial cells of the transformation zone of the cervix. As with other sexually transmitted diseases, the incidence of HPV infection is highest among young women. However, this viral infection is more often than not transient, because most individuals develop an effective type-specific immune response. Approximately 1% of the population has genital warts and 4% of women have cervical precancerous lesions: low grade squamous intraepithelial lesion (LGSIL) or high grade SIL. These last lesions preferentially observed in women aged 35-40 yrs are at high risk of progression towards an invasive cancer. ONCOGENIC POTENTIAL OF HPV: Pre-malignant and malignant cells arise as a result of HPV DNA integration in the host cellular genome, and overexpression of the viral E6 and E7 oncogenes. Cells acquire a proliferative advantage by escaping growth control exerted by p53 and p 105Rb. Both cellular proteins are indeed inactivated respectively by E6 and E7 proteins. Aneuploidy and karyotypic abnormalities are also key events in the tumor progression. A PREVENTABLE DISEASE: Cervical cancer is more than ever a preventable disease. While waiting for clinically applicable vaccination programs, strategies to prevent cervical cancer include 1) improved screening covering the widest possible population and using HPV testing, 2) close management and follow-up of women with precancerous lesions.
Mougin
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Laboratoire de Virologie-Biologie Cellulaire, EA 2085, Faculté de Médecine, Place Saint-Jacques, F 25000 Besançon. christiane.mougin@ufc-chu.univ-fcomte.fr
Dalstein
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V
Prétet
J L
JL
Gay
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Schaal
J P
JP
Riethmuller
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D000328:Adult; D000367:Age Factors; D002294:Carcinoma, Squamous Cell / Q000453:epidemiology / Q000209:etiology / Q000821:virology*; D002471:Cell Transformation, Neoplastic; D004279:DNA, Viral; D005260:Female; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D015994:Incidence; D008403:Mass Screening; D008875:Middle Aged; D009857:Oncogenes / Q000235:genetics; D027383:Papillomaviridae / Q000235:genetics / Q000472:pathogenicity*; D030361:Papillomavirus Infections / Q000150:complications* / Q000453:epidemiology*; D015995:Prevalence; D014412:Tumor Virus Infections / Q000150:complications* / Q000453:epidemiology*; D002583:Uterine Cervical Neoplasms / Q000209:etiology / Q000821:virology*; D002578:Uterine Cervical Dysplasia / Q000453:epidemiology / Q000209:etiology / Q000821:virology*
D004279:DNA, Viral