人乳头瘤病毒致皮肤肿瘤机制的研究进展

Update of HPV-induced skin neoplasm

人乳头瘤病毒(HPV)是一种环状双链DNA病毒,具有噬上皮特性,分为高危型和低危型两类,分别能导致上皮细胞的良性增生与恶变,E5、E6、E7蛋白,L1/L2衣壳蛋白参与高危型HPV引起上皮细胞恶性肿瘤的机制。E6蛋白可抑制PDZ蛋白、Daxx蛋白等抑癌蛋白的作用,激活端粒酶导致细胞永生化,E7蛋白主要通过引起多条信号通路紊乱、介导免疫逃逸、影响多种原癌基因的mi-RNA转录诱导上皮细胞恶变。而E5蛋白、L1/L2衣壳蛋白主要作用是增强E6与E7蛋白的致癌性。本文对人乳头瘤病毒致皮肤肿瘤机制研究进展进行综述。

Human papillomavirus(HPV)is a circular double-stranded DNA virus with phagocytic properties.HPV is classified as high-risk and low-risk types according to the pathogenicity,which can respectively lead to benign hyperplasia and malignant transformation of epithelial cells.E5,E6,E7 and L1/L2 capsid proteins are generally involved in carcinogenesis and E6 may inhibit the function of PDZ and Daxx protein,E7 protein affect the transcription of a variety of mi-RNA through making the multiple signal pathways disorder and mediates immune escape.E5 protein and L1/L2 capsid protein can enhance the carcinogenesi of E6 and E7 protein.The update mechanism of HPV-induced skin tumor is reviewed in this paper.