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Human Papillomavirus (HPV) Type Distribution in Korean Women: A Meta-Analysis.

Korean Women, Meta Analysis, Distribution in Korean, Distribution, Human Papillomavirus, HPV No Comments

 

Department of Obstetrics and Gynecology,The Catholic University of Korea, College of Medicine, Catholic Medical Center, Seoul 000-000, Korea.

The aim of the present study is to estimate the overall prevalence and type distribution of human papillomavirus (HPV) in Korean women, through literature review and metaanalysis. We searched published data for the period between 1995 and 2007 using the following inclusion criteria; (1) studies using type-specific HPV tests, (2) data from Korean female, (3) with cytologic or pathologic results, (4) having more than 20 cases for each subgroup classified by cytologic results, and (5) HPV detection including types 16, 18, and at least one other type. In total, 18 studies (13,842 cases) published up to April 2007 were identified and selected. Adjusted overall HPV prevalence was 23.9% (95% CI: 23.8-24.1%) in women with normal cytology and 95.8% (95% CI: 95.4-96.2%) in women with cervical cancer. Type 16 was predominant regardless of cervical disease status, and type 58 occupied a significantly larger proportion in high-grade cervical intraepithelial lesions and cervical cancer in Korean women. HPV types 58, 33, and 52 together accounted for about 20% of infections in cervical cancer and high-grade intraepithelial lesions. After introduction of HPV prophylactic vaccines, extended protection, especially against types 58, 33, and 52, will be an important issue for cervical cancer prevention in Korea. The future dominant genotypes will require follow-up epidemiological studies with a large-scale, multicentered, and prospective design.

Virological and carcinogenic aspects of HPV

HPV 1 Comment

 

EA 3181, IFR 133, Université de Franche-Comté, Laboratoire de Biologie Cellulaire et Moléculaire, CHU Jean Minjoz, 25030 Besançon.

Human papillomaviruses are small viruses belonging to the Papillomaviridae. More than 100 genotypes have been identified, causing benign (low-risk HPV) or malignant (high-risk HPV) cutaneous or mucosal lesions. The low-risk HPV6 and HPV11 provoke genital warts, while the high-risk HPV16 and HPV18 can cause cervical cancer. The HPVgenome includes several open reading frames that encode proteins involved in viral DNA replication (E1 and E2), viral gene expression regulation (E2), virus assembly (E4) and the immortalisation and transformation of infected epithelial cells (E5, E6 and E7; high-risk HPV only). The open reading frames L1 and L2 encode the two capsid proteins. HPV target stem cells of the squamous epithelium. The complete life cycle involves three phases, with sequential expression of viral genes leading to viral DNA replication and to the production of highly infectious virions. Viral DNA integration occurs with high-risk types and leads to the overexpression of two viral oncoproteins, E6 and E7. These proteins, in combination with E5, promote the immortalisation and transformation of infected cells.

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