摘要
获得性免疫缺陷综合征(AIDS),又称"艾滋病",是威胁着人类生命健康的重大传染性疾病。趋化性细胞因子受体5(Chemotactic cytokine receptor 5,CCR5)作为嗜巨噬细胞性1型人类免疫缺陷病毒(Human immunodeficiency virus type 1,HIV-1)进入宿主细胞的必需的辅助受体自发现以来被广泛关注。CCR5在HIV靶细胞表面的表达水平与靶细胞的病毒载量呈正相关且和艾滋病的进程强相关。因此,通过干预CCR5在靶细胞表面的表达能在一定程度上阻止HIV进入靶细胞。因此,本文从分子水平阐述干预CCR5的主要生物学机制,并对近几年的研究进行综述。
Acquired immunodeficiency syndrome(AIDS)is a major infectious disease that threatens human health.Chemokine cytokine receptor(CCR)5 has attracted extensive attention because it is a necessary accessory receptor for macrophage-like human immunodeficiency virus(HIV)-1 to enter host cells.CCR5 expression on the surface of HIV target cells is correlated positively with the viral load of target cells,and correlated strongly with AIDS progression.Therefore,by inhibiting CCR5 expression on the surface of a target cell,the HIV can be controlled(to a certain extent)to enter the target cell and affect AIDS progression.We reviewed the research results in recent years from studies on the molecular mechanisms that affected CCR5 expression on the surface of target cells.
作者
郑文锦
冯龙
李志慧
ZHENG Wenjin;FENG Long;LI Zhihui(Basic Medical College(Zhongjing College),Henan University of Chinese Medicine,Zheiigzhou 450046,China)
出处
《病毒学报》
CAS
CSCD
北大核心
2021年第1期219-225,共7页
Chinese Journal of Virology
基金
国家自然科学基金(项目号:81503677),题目:针对HIV-1和CXCR4/CCR5启动子为靶点的抗HIV/AIDS药物筛选系统的建立
河南省青年骨干教师资助项目(项目号:2015GGJS-095),题目:穿心莲提取物对外周血CD4^(+)T淋巴细胞表面CXCR4和CCR5的影响及其作用机制的研究
河南省高校重点科研项目(项目号:20A310008),题目:姜黄素调控Foxp3干预人趋化性细胞因子CCR5启动子机制的研究。