Human Papillomavirus in Genital Carcinogenesis

• Published in: Sexually transmitted diseases 1994-03, Vol.21 (2), p.S86-S89
• Main Author: Syrjanen, Kari J
• Format: Article
• Language: English
• Subjects: Biological and medical sciences; Cervical cancer; Deoxyribonucleic acid; DNA; Female; Genital Neoplasms, Female - therapy; Genital Neoplasms, Female - virology; Human viral diseases; Humans; Infectious diseases; Male; Medical research; Medical sciences; Medical screening; Papillomaviridae; Papillomavirus Infections - diagnosis; Papillomavirus Infections - epidemiology; Papillomavirus Infections - therapy; Public health; Sexually transmitted diseases; Sexually Transmitted Diseases, Viral - diagnosis; Sexually Transmitted Diseases, Viral - epidemiology; STD; Tumor Virus Infections - diagnosis; Tumor Virus Infections - epidemiology; Tumor Virus Infections - therapy; Viral diseases; Viral diseases of the genital and urinary system
• ISSN: 0148-5717; 1537-4521

Human papillomavirus (HPV) is known to induce three different manifestations: clinical, subclinical, and latent infection. Clinical infections (exophytic, endophytic, or flat condylomas) frequently are associated with intraepithelial neoplasia and invasive squamous cell cancer. Colposcopy, cytology, and histopathology play a central role in diagnosis of clinical HPV infections, whereas DNA hybridization techniques and DNA amplification with polymerase chain reaction (PCR) are needed to detect the subclinical and latent HPV infections. The biologic behavior of genital HPV infections is a complex one: regression, persistence, progression, and fluctuation are recognized disease patterns. In young women, the prevalence of HPV infections in Papanicolaou smears is 3%, and the annual incidence approximately 8%. The lifetime risk approaches 80% for women between 20 and 80 years of age. The number of sexual partners during the past 2 years (relative risk [RR] > 9.0) and current smoking (RR > 5.0) proved to be the two most significant risk factors for clinical HPV infection in a recent casecontrol study. In the author's prospective follow-up study, clinical progression was significantly related to the grade of HPV lesion (P < 0.0001), and to HPV type, with the progression rate of HPV 16 lesions being more than five times greater than that of HPV 6 or 11 lesions. The detection rate of HPV in men is significantly lower (approximately 30%) than in women, and the concordance of HPV types in the couples having sexual relations is surprisingly low (5% to 10%). To reduce the worldwide incidence of cervical cancer (>600,000 cases a year), it would be better to establish covering, mass-screening programs in high-risk countries than to introduce sophisticated DNA or PCR technology to screen large populations for subclinical and latent HPV infections.