人乳头瘤病毒致癌机制的研究进展

Current Advances in the Mechanic Studies of Human Papillomavirus-induced Oncogenesis

人乳头瘤病毒(HPV)是一种常见的小DNA双链病毒,主要感染上皮黏膜细胞,引起良性乳头瘤病变和恶性肿瘤,高危型HPV在子宫颈癌组织中的检出率可高达90%以上。E6和E7是HPV最重要的两个病毒癌基因,在病毒整合入宿主细胞基因组后可持续表达,并分别与细胞内重要的抑癌基因p53和pRb的蛋白产物相互作用,阻遏其对细胞增殖分化的负调控,从而诱发细胞恶性转化。此外,E6和E7表达还可影响基因组稳定性。

Human papillomavirus （HPV） is a common small DNA tumor virus that specifically infects squamous epithelial cells and causes benign or malignant epithelial lesions such as genital warts and cervical cancer. High-risk HPV is detected in specimens of more than 90% of cervical cancer. In the 7.9 kb genome of HPV, E6 and E7 are the crucial viral oncoproteins that consistently maintained after viral integration into host cell genome. These two proteins interfere with cell proliferation and differentiation through interacting with important tumor suppressors including p53 and pRb. High-risk HPV E6/E7 also induces genomic instability, cilitating cell transformation.