Virion Infectivity(病毒粒子传染性)研究综述
Virion Infectivity 病毒粒子传染性 - Our findings indicate that the Vpr-TET2 axis enhances HIV-1 replication in macrophages via two independent mechanisms: reduced IFTIM3 expression to enhance Env processing and virion infectivity and sustained IL-6 expression to increase HIV-1 replication. [1] The N-terminal region in HIV-1 Nef encompassing residues 12 to 39 has been implicated in many Nef activities, including disruption of CD4 T lymphocyte polarization and homing to lymph nodes, antagonism of SERINC5 restriction to virion infectivity, downregulation of cell surface CD4 and major histocompatibility complex class I (MHC-I), release of Nef-containing extracellular vesicles, and phosphorylation of Nef by recruitment of the Nef-associated kinase complex (NAKC). [2] In addition to these anti-cancer properties, man-specific seaweed lectins have been widely used as potent human immunodeficiency virus (HIV-1)-inactivating proteins, due to their capacity to specifically interact with the envelope glycoprotein gp120 and prevent the virion infectivity of HIV-1 towards the host CD4+ T-lymphocyte cells in vitro. [3] The accurate and efficient cleavage of Gag is essential for virion infectivity; inhibitors of the viral protease are potent antivirals, and substitutions in Gag that prevent its cleavage result in reduced HIV-1 infectivity. [4]我们的研究结果表明，Vpr-TET2 轴通过两种独立的机制增强巨噬细胞中的 HIV-1 复制：降低 IFTIM3 表达以增强 Env 加工和病毒粒子感染性，以及持续 IL-6 表达以增加 HIV-1 复制。 [1] HIV-1 Nef 的 N 末端区域包含 12 至 39 位残基，与许多 Nef 活性有关，包括 CD4 T 淋巴细胞极化和归巢到淋巴结的破坏、SERINC5 限制对病毒粒子感染性的拮抗、细胞表面 CD4 的下调和主要组织相容性复合物 I 类 (MHC-I)，释放含有 Nef 的细胞外囊泡，以及通过募集 Nef 相关激酶复合物 (NAKC) 使 Nef 磷酸化。 [2] 除了这些抗癌特性外，人类特异性海藻凝集素已被广泛用作有效的人类免疫缺陷病毒 (HIV-1) 灭活蛋白，因为它们能够与包膜糖蛋白 gp120 特异性相互作用并防止病毒粒子的感染性。 HIV-1 在体外针对宿主 CD4+ T 淋巴细胞。 [3] Gag 的准确和有效切割对于病毒粒子的感染性至关重要；病毒蛋白酶抑制剂是有效的抗病毒药物，Gag 中阻止其裂解的替代物会导致 HIV-1 感染性降低。 [4]
virion infectivity factor 病毒感染因子
Introduction: Virion Infectivity factor (Vif) is a protein required for lentiviruses successful infection of human target cells, through the degradation of host restriction factors, APOBEC3 [1]. [1] HIV-1 virion infectivity factor (Vif) promotes degradation of the antiviral APOBEC3 (A3) proteins through the host ubiquitin-proteasome pathway to enable viral immune evasion. [2]简介：病毒粒子感染因子（Vif）是慢病毒成功感染人体靶细胞所需的蛋白质，通过降解宿主限制因子APOBEC3[1]。 [1] HIV-1病毒粒子感染因子（Vif）通过宿主泛素-蛋白酶体途径促进抗病毒APOBEC3（A3）蛋白的降解，从而实现病毒免疫逃避。 [2]