摘要
获得性免疫缺陷综合征(acquired immune deficiency syndrome,AIDS)是一种由人类免疫缺陷病毒(HIV)引发的全身性疾病。趋化因子配体3[Chemokine(C-C motif)ligand 3,CCL3]作为趋化因子家族的重要成员,在艾滋病发病机制中扮演着不可或缺的角色。CCL3通过阻止HIV进入靶细胞,激活免疫细胞增强抗病毒能力,并调节炎症反应和影响疾病进展,发挥重要的抗病毒和免疫调节作用。大量研究表明CCL3基因拷贝数、特定T细胞反应、CCL3多态性以及其参与的信号通路均影响HIV的发展及病毒载量。综述了CCL3通过阻断HIV-1进入免疫细胞、诱导抗病毒蛋白表达抑制病毒复制,以及其多态性和等位基因对HIV感染及进展的影响等多方面对艾滋病的作用,以期为艾滋病防治策略提供新的理论支撑。
Acquired immune deficiency syndrome(AIDS)is a systemic disease caused by the Human Immunodeficiency Virus(HIV).Chemokine(C-C motif)ligand 3(CCL3),as a vital member of the chemokine family,plays an indispensable role in the pathogenesis of AIDS.In the context of AIDS,CCL3 exerts significant antiviral and immunomodulatory effects by preventing HIV entry into target cells,activating immune cells to enhance antiviral capabilities,and modulating inflammatory responses,thereby influencing disease progression.Numerous studies have demonstrated that CCL3 gene copy number,specific T-cell responses,CCL3 polymorphisms,and the signaling pathways it participates in all influence the development of HIV and viral load.This article comprehensively reviews the multifaceted roles of CCL3 in AIDS,including its ability to block HIV-1 entry into immune cells,inducing the expression of antiviral proteins to inhibit viral replication,as well as the influence of its polymorphisms and alleles on HIV infection and disease progression,aiming to provide novel theoretical support for AIDS prevention and treatment strategies.
作者
刘元菊
李晓岚
刘洁
许银德
朱芸
LIU Yuanju;LI Xiaolan;LIU Jie;XU Yinde;ZHU Yun(Department of Dermatology&STD,The Second Affiliated Hospital of Kunming Medical University,Kunming Yunnan 650101,China)
出处
《昆明医科大学学报》
2025年第2期1-8,共8页
Journal of Kunming Medical University
基金
国家自然科学基金(81760136)
硕士研究生创新基金(2024S274)。
关键词
趋化因子
CCL3
艾滋病
Chemokine
Chemokine(C-C motif)ligand 3
Acquired immune deficieny syndrome
