Various strategies for developing APOBEC3G protectors to circumvent human immunodeficiency virus type 1

被引：0
|
作者：
Bao, Qiqi [1 ,2 ]
Zhou, Jinming [1 ,2 ]
机构：
[1] Zhejiang Normal Univ, Dept Chem, Key Lab Minist Educ Adv Catalysis Mat, 688 Yingbin Rd, Jinhua 321004, Peoples R China
[2] Zhejiang Normal Univ, Coll Chem & Life Sci, Drug Dev & Innovat Ctr, 688 Yingbin Rd, Jinhua 321004, Peoples R China
来源：
EUROPEAN JOURNAL OF MEDICINAL CHEMISTRY | 2023年 / 250卷
关键词：
HIV-1; REVERSE-TRANSCRIPTASE; SMALL-MOLECULE INHIBITION; CYTIDINE DEAMINASE; MESSENGER-RNA; ANTIRETROVIRAL THERAPY; ANTIVIRAL ACTIVITY; CBF-BETA; INDEPENDENT RESTRICTION; ENZYME APOBEC3G; INNATE IMMUNITY;
D O I：
10.1016/j.ejmech.2023.115188
中图分类号：
R914 [药物化学];
学科分类号：
100701 ;
摘要：
Host restriction factor APOBEC3G (A3G) efficiently restricts Vif-deficient HIV-1 by being packaged with progeny virions and causing the G to A mutation during HIV-1 viral DNA synthesis as the progeny virus infects new cells. HIV-1 expresses Vif protein to resist the activity of A3G by mediating A3G degradation. This process requires the self-association of Vif in concert with A3G proteins, protein chaperones, and factors of the ubiquitination ma-chinery, which are potential targets to discover novel anti-HIV drugs. This review will describe compounds that have been reported so far to inhibit viral replication of HIV-1 by protecting A3G from Vif-mediated degradation.
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页数：14
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