García-Carrancá A, Gariglio P V
Departamento de Biología Molecular, Universidad Nacional Autónoma de México, D.F.
Rev Invest Clin. 1993 Jan-Feb;45(1):85-92.
Papillomaviruses (wart viruses) are responsible for the development of benign and malignant epithelial lesions in mammals. More than 60 different types of human papillomaviruses (HPVs) have been isolated to date. Some of them are major candidates as etiologic agents in cervical cancer. DNA from HPV types 16, 18 and 33 is usually found integrated in about 90 percent of genital carcinomas. Integration of the viral DNA into the cellular genome may be an important step towards the development of malignancy. Two early genes of HPVs (E6 y E7) are involved in cellular transformation. Another early gene (E2) participates in gene control by directly binding to conserved DNA motifs in the viral genome. Several protein factors of viral and cellular origin interact with the regulatory region of HPVs and participate in the regulation transcription of oncogenes E6 and E7. Cellular factors, such as immune system and oncogene and anti-oncogene alterations, seem to play an important role in papillomavirus-associated cervical carcinogenesis.
乳头瘤病毒（疣病毒）可引发哺乳动物良性和恶性上皮病变。迄今为止，已分离出60多种不同类型的人乳头瘤病毒（HPV）。其中一些是宫颈癌病因的主要候选因素。在约90%的生殖器癌中通常可发现16型、18型和33型HPV的DNA整合。病毒DNA整合到细胞基因组中可能是迈向恶性肿瘤发展的重要一步。HPV的两个早期基因（E6和E7）参与细胞转化。另一个早期基因（E2）通过直接结合病毒基因组中的保守DNA基序参与基因调控。几种病毒和细胞来源的蛋白质因子与HPV的调控区域相互作用，并参与癌基因E6和E7的转录调控。细胞因子，如免疫系统以及癌基因和抗癌基因的改变，似乎在乳头瘤病毒相关的宫颈癌发生过程中起重要作用。
