Virion Release(病毒释放)研究综述
Virion Release 病毒释放 - These changes in the viral condensate upon exogenous stress, accompanied by down-regulation of the host antiviral response, provide an environment that supports up-regulation of viral replication and virion release. [1] Instead of budding, SIFV induces the formation of pyramidal structures, which penetrate the cell envelope and serve as portals for virion release. [2] M inhibits the activity of lysosome protease, and uses autolysosomes for virion release. [3] Our SARS-CoV-2-specific MRA combines the quantitative measurement of several parameters of virus infection, such as the intracellular production of proteins and genomes, enzymatic activities and virion release, as well as the use of reporter systems. [4] Successful viral propagation, including viral entry, immune evasion, virion release and viral spread rely on dynamic molecular interactions with the surfaceome. [5] Viruses exhibit a diverse array of strategies for infecting host cells and for virion release after replication. [6] We show that ORF3's absence substantially decreased HEV replication and virion release from the apical surface but not the basolateral surface of polarized hepatocytes. [7] ABSTRACT The influenza A virus (IAV) neuraminidase (NA) is essential for virion release from cells and decoy receptors and an important target of antiviral drugs and antibodies. [8] Viral proteins recruit over 300 host partners forming hetero-oligomeric complexes enabling the viral RNA synthesis, packing, and virion release. [9] This mechanism of virion release is operating exclusively in cells of hyperthermophilic hosts from the phylum Crenarchaeaota, which are encased solely by a layer of surface proteins, S-layer. [10] Here, we have attempted to address the timing of EV and virion release from virally infected cells. [11] We demonstrated that the antiviral effect of 16 is not related to reduced viral RNA synthesis or virion release. [12] Site-directed mutagenesis of p8, PLPPV, and p14NC, PLPPL, sequences in MMTV Gag revealed a requirement only for the PLPPV sequence in virion release in a position-dependent manner. [13] Instead we report observing multiple rounds of transient recruitment of ALIX, CHMP4 and VPS4 prior to virion release. [14] The small CoV envelope (E) protein plays roles in assembly, virion release, and pathogenesis. [15] Deletion of the gE gene strongly enhanced virus release to the medium in Vero cells, suggesting that the gE-dependent spread pathway may compete with virion release to the medium. [16] ABSTRACT BST-2/CD317/tetherin is a host transmembrane protein that potently inhibits human immunodeficiency virus type 1 (HIV-1) virion release by tethering the nascent virions to the plasma membrane. [17] Inducing Hsp70 expression in mammalian cells increased ZIKV production, whereas inhibiting Hsp70 activity reduced ZIKV viral RNA production and virion release from the cell. [18]外源性应激时病毒凝聚物的这些变化，伴随着宿主抗病毒反应的下调，提供了一个支持病毒复制和病毒粒子释放上调的环境。 [1] SIFV 不是出芽，而是诱导锥体结构的形成，锥体结构穿透细胞包膜并作为病毒粒子释放的入口。 [2] M 抑制溶酶体蛋白酶的活性，并使用自溶酶体释放病毒粒子。 [3] 我们的 SARS-CoV-2 特异性 MRA 结合了病毒感染的几个参数的定量测量，例如蛋白质和基因组的细胞内产生、酶活性和病毒粒子释放，以及报告系统的使用。 [4] 成功的病毒传播，包括病毒进入、免疫逃避、病毒粒子释放和病毒传播，依赖于与表面组的动态分子相互作用。 [5] 病毒表现出多种用于感染宿主细胞和复制后病毒粒子释放的策略。 [6] 我们表明，ORF3 的缺失显着降低了 HEV 复制和病毒粒子从顶端表面的释放，而不是极化肝细胞的基底外侧表面。 [7] 摘要 甲型流感病毒 (IAV) 神经氨酸酶 (NA) 是病毒粒子从细胞和诱饵受体释放所必需的，也是抗病毒药物和抗体的重要靶点。 [8] 病毒蛋白招募超过 300 个宿主伙伴，形成异源寡聚复合物，使病毒 RNA 合成、包装和病毒粒子释放成为可能。 [9] 这种病毒粒子释放机制仅在来自 Crnarchaeaota 门的超嗜热宿主细胞中起作用，这些细胞仅被一层表面蛋白 S 层包裹。 [10] 在这里，我们试图解决病毒感染细胞释放 EV 和病毒粒子的时间。 [11] 我们证明了 16 的抗病毒作用与减少的病毒 RNA 合成或病毒粒子释放无关。 [12] MMTV Gag 中p8、PLPPV 和p14NC、PLPPL 序列的定点诱变揭示了仅对PLPPV 序列以位置依赖性方式释放病毒粒子的要求。 [13] 相反，我们报告在病毒粒子释放之前观察到多轮 ALIX、CHMP4 和 VPS4 的瞬时募集。 [14] 小 CoV 包膜 (E) 蛋白在组装、病毒粒子释放和发病机制中发挥作用。 [15] gE基因的缺失强烈增强了Vero细胞中病毒向培养基的释放，这表明依赖于gE的传播途径可能与病毒粒子向培养基的释放竞争。 [16] 摘要 BST-2/CD317/tetherin 是一种宿主跨膜蛋白，可通过将新生病毒粒子束缚在质膜上来有效抑制人类免疫缺陷病毒 1 型 (HIV-1) 病毒粒子的释放。 [17] 在哺乳动物细胞中诱导 Hsp70 表达会增加 ZIKV 的产生，而抑制 Hsp70 活性会降低 ZIKV 病毒 RNA 的产生和病毒粒子从细胞中的释放。 [18]
Enhanced Virion Release 增强的病毒释放
Previously described mutants that abolish nuclear cycling displayed enhanced plasma membrane binding, enhanced virion release, and a significant loss in genome incorporation resulting in loss of infectivity. [1] Previously described mutants that abolish nuclear cycling displayed enhanced plasma membrane binding, enhanced virion release, and a significant loss in genome incorporation resulting in loss of infectivity. [2]先前描述的消除核循环的突变体显示出增强的质膜结合、增强的病毒粒子释放和基因组整合的显着损失，从而导致感染性丧失。 [1] 先前描述的消除核循环的突变体显示出增强的质膜结合、增强的病毒粒子释放和基因组整合的显着损失，从而导致感染性丧失。 [2]
Decreased Virion Release 减少病毒粒子释放
Moreover, asunaprevir profoundly decreased virion release from SARS-CoV-2-infected cells. [1] Moreover, asunaprevir profoundly decreased virion release from SARS-CoV-2-infected cells. [2]此外，阿舒瑞韦显着降低了 SARS-CoV-2 感染细胞中病毒粒子的释放。 [1] 此外，阿舒瑞韦显着降低了 SARS-CoV-2 感染细胞中病毒粒子的释放。 [2]
Abrogating Virion Release 取消病毒粒子释放
Of note, in PHHs, HCV infection initiated broad upregulation of canonical interferon (IFN)-mediated defense programs, limiting viral RNA replication and abrogating virion release. [1] Of note, in PHHs, HCV infection initiated broad upregulation of canonical interferon (IFN)-mediated defense programs, limiting viral RNA replication and abrogating virion release. [2]值得注意的是，在 PHH 中，HCV 感染引发了经典干扰素 (IFN) 介导的防御程序的广泛上调，限制了病毒 RNA 复制并消除了病毒粒子的释放。 [1] 值得注意的是，在 PHH 中，HCV 感染引发了经典干扰素 (IFN) 介导的防御程序的广泛上调，限制了病毒 RNA 复制并消除了病毒粒子的释放。 [2]
2 Virion Release 2 病毒粒子释放
This was particularly striking when both IRE1α and ATF6 branches of the UPR were inhibited, reducing SARS-CoV-2 virion release (~1,000-fold). [1] This was particularly striking when both IRE1α and ATF6 branches of the UPR were inhibited, reducing SARS-CoV-2 virion release ∼1,000-fold. [2]当 UPR 的 IRE1α 和 ATF6 分支都被抑制时，这一点尤其引人注目，从而减少了 SARS-CoV-2 病毒粒子的释放（约 1,000 倍）。 [1] 当 UPR 的 IRE1α 和 ATF6 分支都被抑制时，这一点尤其引人注目，将 SARS-CoV-2 病毒粒子的释放减少了约 1,000 倍。 [2]