不同的宿主蛋白靶向不同的HIV蛋白并拮抗它们的功能,取决于HIV生命周期的阶段和感染阶段。同时,HIV蛋白还靶向和拮抗各种不同的宿主蛋白以促进HIV在宿主细胞内的复制。前面相当具体的知识领域在艾滋病毒的发病机理,然而,仍然没有得到足够的理解。因此,我们建议,在这篇评论文章中,研究和讨论对抗那些直接导致HIV感染性增加的宿主限制性蛋白的HIV蛋白。我们详细阐述了拮抗宿主细胞蛋白以促进HIV复制的HIV蛋白,从而感染艾滋病毒。我们研究了Nef的功能和机制,Vif,Vpu,Env,Vpr,和Vpx抵消宿主蛋白,如Ser5,PSGL-1,IFITMS,A3G,Tetherin,GBP5,SAMHD1,STING,HUSH,REAF,和TET2增加艾滋病毒的传染性。Nef拮抗三种宿主蛋白,viz.,Ser5、PSGL1和IFITIM,而Vpx还拮抗三种宿主限制因子,viz.,SAMHD1,STING,和HUSH复合体;因此,这些蛋白可能是HIV感染治疗干预的潜在候选蛋白.Tetherin是Vpu和Env的目标,PSGL1是Nef和Vpu的目标,而Ser5由Nef和Env蛋白靶向。最后,还提出了结论性意见和未来观点。
Different host proteins target different HIV proteins and antagonize their functions, depending on the stage of the HIV life cycle and the stage of infection. Concurrently, HIV proteins also target and antagonize various different host proteins to facilitate HIV replication within host cells. The preceding quite specific area of knowledge in HIV pathogenesis, however, remains insufficiently understood. We therefore propose, in this review article, to examine and discuss the HIV proteins that counteract those host restriction proteins which results directly in increased infectivity of HIV. We elaborate on HIV proteins that antagonize host cellular proteins to promote HIV replication, and thus HIV infection. We examine the functions and mechanisms via which Nef, Vif, Vpu, Env, Vpr, and Vpx counteract host proteins such as Ser5, PSGL-1, IFITMS, A3G, tetherin, GBP5, SAMHD1, STING, HUSH, REAF, and TET2 to increase HIV infectivity. Nef antagonizes three host proteins, viz., Ser5, PSGL1, and IFITIMs, while Vpx also antagonizes three host restriction factors, viz., SAMHD1, STING, and HUSH complex; therefore, these proteins may be potential candidates for therapeutic intervention in HIV infection. Tetherin is targeted by Vpu and Env, PSGL1 is targeted by Nef and Vpu, while Ser5 is targeted by Nef and Env proteins. Finally, conclusive remarks and future perspectives are also presented.