面对HPV持续感染使宫颈病变风险增加250倍，而HPV(-)和HPV(+)在基因层次上又未见明显差异，临床上对HPV感染的治疗手段又极其缺乏的现状，深入研究HPV感染导致宫颈病变的发病机制，探索安全有效的防治方法具有非常重要的意义。本项目首先从蛋白层次入手，选取仅针对HPV16阳性患者的宫颈组织，应用质谱技术进行蛋白组学分析，结合生物信息学分析，发现在宫颈病变的过程中，VAMP7蛋白表达变化呈先下降后升高的趋势，同时SNARE相关蛋白也有显著性差异。所以本项目提出科学假说，在HPV16感染初期，VAMP7低表达抑制细胞自噬，而随着病变进展，VAMP7表达升高自噬过程恢复，但病变细胞无法被清除，最终导致严重不可逆病变。本项目拟通过研究VAMP7对宫颈细胞功能的影响及其相关信号通路对细胞自噬过程的调控机制，VAMP7在宫颈病变进展过程中的作用，探寻防治HPV16感染引起的宫颈病变的方法。

In the face of persistent infection with the HPV can make 250 times increased risk of cervical lesions. No obvious difference between HPV (-) and HPV (+) at the genetic level shown the lack of clinical treatment for HPV infection. The machnism of HPV infection in the pathogenesis of cervical disease, to explore a safe and effective method of prevention has the very important significance. First of all, from the perspective of the protein level, only selected in view of the HPV16 group, application of mass spectrometry analysis of proteomics, bioinformatics analysis, found in the process of the cervical lesions, VAMP7 protein expression changes into decline after rising first, but all the lesions were higher than in group negative group, and SNARE related proteins also have significant differences.Therefore, this project proposes a scientific hypothesis that, in the early stage of HPV16 infection, low VAMP7 expression inhibits the autophagy process, while as the lesion progresses, high VAMP7 expression increases the autophagy process, but the diseased cells cannot be removed, eventually lead to serious irreversible lesions.This project intends to explore the role of VAMP7 in the progression of cervical lesions by studying the effect of VAMP7 on the function of cervical cells and the regulatory mechanism of relevant signaling pathways on the process of autophagy, so as to explore and find the method to prevent and treat cervical lesions caused by HPV16.