Monocyte/Macrophage-Mediated Innate Immunity in HIV-1 Infection:From Early Response to Late Dysregulation and Links to Cardiovascular Diseases Onset  

作　　者：Eman Teer Danzil E.Joseph Richard H.Glashoff M.Faadiel Essop 

机构地区：[1]Centre for Cardio-metabolic Research in Africa(CARMA),Department of Physiological Sciences,Stellenbosch University,Stellenbosch 7600,South Africa [2]Division of Medical Microbiology&Immunology,Department of Pathology,Stellenbosch University and NHLS,Cape Town 7505,South Africa

出　　处：《Virologica Sinica》2021年第4期565-576,共12页中国病毒学（英文版）

摘　　要：Although monocytes and macrophages are key mediators of the innate immune system,the focus has largely been on the role of the adaptive immune system in the context of human immunodeficiency virus(HIV)infection.Thus more attention and research work regarding the innate immune system-especially the role of monocytes and macrophages during early HIV-1 infection-is required.Blood monocytes and tissue macrophages are both susceptible targets of HIV-1 infection,and the early host response can determine whether the nature of the infection becomes pathogenic or not.For example,monocytes and macrophages can contribute to the HIV reservoir and viral persistence,and influence the initiation/extension of immune activation and chronic inflammation.Here the expansion of monocyte subsets(classical,intermediate and non-classical)provide an increased understanding of the crucial role they play in terms of chronic inflammation and also by increasing the risk of coagulation during HIV-1 infection.This review discusses the role of monocytes and macrophages during HIV-1 pathogenesis,starting from the early response to late dysregulation that occurs as a result of persistent immune activation and chronic inflammation.Such changes are also linked to downstream targets such as increased coagulation and the onset of cardiovascular diseases.

关 键 词：MONOCYTES Human immunodeficiency virus(HIV) Persistent immune activation COAGULATION Cardiovascular diseases(CVD) 

分 类 号：R392[医药卫生—免疫学]