HPV致宫颈癌机制研究进展

人乳头瘤病毒（human papillomavirus, HPV）是一类无包膜的具有嗜上皮特性的双链DNA病毒，由核酸及衣壳蛋白构成，其基因组可分为早期编码区（E区）、晚期编码区（L区）和长控制区（LCR），研究表明高危型HPV的持续感染与宫颈癌的发生密切相关，当HPV病毒感染机体后，其基因组可随机整合到宿主细胞DNA中，随后沉默E2基因的表达，削弱E2蛋白对E6、E7基因的抑制，使E6、E7蛋白过表达，辅以E5蛋白的表达，促使感染细胞永生化甚至癌变。因此研究HPV的病毒结构及其致病机制对防治HPV感染及预防HPV相关恶性肿瘤，尤其是宫颈癌的发生、发展尤为重要。本文拟就HPV的病毒结构、致病机制研究进展进行综述。

Advances on the carcinogenetic mechanisms of HPV in cervical cancer

Human papillomavirus(HPV) is a type of non-enveloped double-stranded DNA virus with epithelialophilic properties. The HPV virus is composed of nucleic acid and capsid protein, and its genome consists of early coding region(E region), late coding region(L region) and long control region(LCR). Studies have shown that persistent infection of high-risk HPV is closely related to the occurrence of cervical cancer. After HPV infected the body, its genome is randomly integrated into the DNA of host cell, then silences the expression of E2 gene, weakens the inhibition of E2 protein on E6 and E7 genes, makes E6 and E7 proteins over-expressed, complemented with the expression of E5 protein to promote the immortalization or canceration of infected cells. Therefore, studying the viral structure and pathogenesis of HPV is particularly important for the prevention and treatment of HPV infection and prevention of HPV-related malignancies, especially the occurrence and development of cervical cancer. This article reviews the research progress on the structure of HPV and its mechanism in carcinogenesis of cervical cancer.