Virus Fusion(病毒融合)研究综述
Virus Fusion 病毒融合 - Using both reconstituted and native cell membranes as materials to functionalize organic bioelectronic devices, configured as electrodes and transistors, we measure changes in membrane properties when virus fusion is triggered by a pH drop, inducing hemagglutinin to undergo a conformational change that leads to membrane fusion. [1] The matured functional spike glycoprotein is presented on the virion surface as trimers, which contain two subunits, such as S1 (virus attachment) and S2 (virus fusion). [2] Further exploring the star-shaped features may provide new molecular alternatives to cross-bind the α-helices of S-SLSF to hypothetically inhibit coronavirus fusion. [3] To gain insights into arenavirus fusion, we examined cell-cell fusion induced by the Old World Lassa virus (LASV) GPC complex. [4] Reovirus fusion-associated small transmembrane (FAST) proteins induce syncytium formation. [5] By decreasing the probability of virus fusion In the body and some other useful ways. [6] Altogether, our structural and morphological data support a cholesterol-dependent conformational plasticity for this HIV-1 sequence, which could assist cell-virus fusion by destabilizing the viral membrane at the initial stages of the process. [7] To gain insights into arenavirus fusion, we examined cell-cell fusion induced by the Old World Lassa virus (LASV) GPC complex. [8] These insights should enable the inclusion of the conformations of the spike protein transmembrane domain into the prevalent models of virus fusion. [9] ON-1 Iranian sequences clustered in three lineages according to virus fusion (F) gene variations. [10] We found that cells with a lower ATP:ADP ratio prior to virus addition were less permissive to virus fusion and infection. [11] Together, our results strongly support a model according to which IFITM3 accumulation at the sites of virus fusion is a prerequisite for its antiviral activity and that this protein traps viral fusion at a hemifusion stage by preventing the formation of fusion pores. [12] In this study, by comparatively analyzing the mechanisms of baculovirus entry into mammalian and insect cells, virus fusion during the early stage of endocytosis was revealed as the major obstacle for efficient baculovirus transduction into mammalian cells. [13] Unraveling the molecular mechanism of herpesvirus fusion has been a goal of fundamental research for years, and yet important mechanistic details remain to be uncovered. [14]我们使用重组和天然细胞膜作为材料来功能化配置为电极和晶体管的有机生物电子设备，我们测量了当 pH 值下降触发病毒融合时膜特性的变化，从而诱导血凝素经历导致膜融合的构象变化。 [1] 成熟的功能性刺突糖蛋白以三聚体形式呈现在病毒粒子表面，其中包含两个亚基，例如 S1（病毒附着）和 S2（病毒融合）。 [2] 进一步探索星形特征可能会提供新的分子替代品 交叉结合 S-SLSF 的 α 螺旋以假设抑制冠状病毒融合。 [3] 为了深入了解沙粒病毒融合，我们检查了由旧世界拉沙病毒 (LASV) GPC 复合物诱导的细胞 - 细胞融合。 [4] 呼肠孤病毒融合相关小跨膜 (FAST) 蛋白诱导合胞体形成。 [5] 通过降低病毒在体内融合的概率等一些有用的方法。 [6] 总之，我们的结构和形态数据支持这种 HIV-1 序列的胆固醇依赖性构象可塑性，这可以通过在过程的初始阶段破坏病毒膜来帮助细胞-病毒融合。 [7] 为了深入了解沙粒病毒融合，我们检查了由旧世界拉沙病毒 (LASV) GPC 复合物诱导的细胞 - 细胞融合。 [8] 这些见解应该能够将刺突蛋白跨膜结构域的构象纳入流行的病毒融合模型中。 [9] 根据病毒融合 (F) 基因变异，ON-1 伊朗序列聚集在三个谱系中。 [10] 我们发现在添加病毒之前具有较低 ATP:ADP 比率的细胞对病毒融合和感染的允许性较低。 [11] 总之，我们的结果强烈支持一个模型，根据该模型，IFITM3 在病毒融合位点的积累是其抗病毒活性的先决条件，并且该蛋白通过阻止融合孔的形成在半融合阶段捕获病毒融合。 [12] 本研究通过对比分析杆状病毒进入哺乳动物和昆虫细胞的机制，揭示了胞吞作用早期的病毒融合是杆状病毒有效转入哺乳动物细胞的主要障碍。 [13] 多年来，揭示疱疹病毒融合的分子机制一直是基础研究的目标，但重要的机制细节仍有待发现。 [14]
target cell binding 靶细胞结合
SARS-CoV-2 virions are surrounded by a lipid bilayer which contains membrane proteins such as Spike, responsible for target-cell binding and virus fusion, the envelope protein E and the accessory protein Orf3a. [1] SARS-CoV-2 virions are surrounded by a lipid bilayer that contains membrane proteins such as spike, responsible for target-cell binding and virus fusion. [2] SARS-CoV-2 virions are surrounded by a lipid bilayer which contains membrane proteins such as Spike, responsible for target-cell binding and virus fusion, the envelope protein E and the accessory protein Orf3a. [3]SARS-CoV-2 病毒粒子被脂质双层包围，该脂质双层包含负责靶细胞结合和病毒融合的膜蛋白如 Spike、包膜蛋白 E 和辅助蛋白 Orf3a。 [1] SARS-CoV-2 病毒粒子被脂质双层包围，该脂质双层含有膜蛋白，如刺突蛋白，负责靶细胞结合和病毒融合。 [2] nan [3]
Syncytial Virus Fusion 合胞病毒融合
Aluminum phosphate was used in Respiratory Syncytial Virus Fusion candidate vaccines (n=3) and Tdap vaccines (n=3). [1] Here, we generated a new set of LNPs whose surface was modified with mannans of different length (from mono to tetrasaccharide), in order to study the effect on antibody response of model SAM replicon encoding for the respiratory syncytial virus fusion F protein. [2] Introduction The study objective was to characterize the excretion and metabolic profile of the respiratory syncytial virus fusion protein inhibitor, JNJ-53718678. [3] The respiratory syncytial virus fusion (RSV‐F) protein is a primary target for vaccine and drug development against respiratory infection and pediatric pneumonia. [4]磷酸铝用于呼吸道合胞病毒融合候选疫苗 (n=3) 和 Tdap 疫苗 (n=3)。 [1] 在这里，我们生成了一组新的 LNP，其表面用不同长度的甘露聚糖（从单糖到四糖）进行了修饰，以研究编码呼吸道合胞病毒融合 F 蛋白的模型 SAM 复制子对抗体反应的影响。 [2] 简介 本研究的目的是描述呼吸道合胞病毒融合蛋白抑制剂 JNJ-53718678 的排泄和代谢特征。 [3] 呼吸道合胞病毒融合 (RSV-F) 蛋白是针对呼吸道感染和小儿肺炎的疫苗和药物开发的主要靶点。 [4]
Influenza Virus Fusion
Our study describes ADE with two different functional MAbs that destabilized HA stem domain, increased influenza virus fusion kinetics, and led to enhanced lung pathology and ERD in a dose-dependent manner in a mice model. [1] 5]decan‐4‐yl)‐carboxamide compounds carrying the 5‐chloro‐2‐methoxybenzamide structure, designed as influenza virus fusion inhibitors. [2] Compound 8n and structural analogs were devoid of anti‐influenza virus activity, although their scaffold is shared with a previously discovered class of H3 hemagglutinin‐specific influenza virus fusion inhibitors. [3]我们的研究描述了 ADE 与两种不同的功能性 MAb，它们破坏了 HA 干结构域的稳定性，增加了流感病毒融合动力学，并在小鼠模型中以剂量依赖性方式导致肺病理学和 ERD 增强。 [1] 5]癸-4-基)-甲酰胺化合物，具有5-氯-2-甲氧基苯甲酰胺结构，设计为流感病毒融合抑制剂。 [2] 化合物 8n 和结构类似物缺乏抗流感病毒活性，尽管它们的支架与先前发现的一类 H3 血凝素特异性流感病毒融合抑制剂共享。 [3]
Dengue Virus Fusion
We propose a 2-step mechanism for the interaction of the dengue virus fusion peptide with the host membrane, where the N-terminal sequence docks electrostatically on the headgroups and then the C-terminal interacts via hydrophobic forces in the acyl chains. [1] In this review, we summarize some of the basic NMR structure based approaches and techniques which aid in improving the activity of AMPs, using the example of a 16-residue dengue virus fusion protein derived peptide, VG16KRKP. [2]我们提出了登革病毒融合肽与宿主膜相互作用的两步机制，其中 N 端序列静电停靠在头部基团上，然后 C 端通过酰基链中的疏水力相互作用。 [1] 在这篇综述中，我们以 16 残基登革热病毒融合蛋白衍生肽 VG16KRKP 为例，总结了一些基于 NMR 结构的基本方法和技术，这些方法和技术有助于提高 AMP 的活性。 [2]
Enveloped Virus Fusion 包膜病毒融合
Cholesterol serves critical roles in enveloped virus fusion by modulating membrane properties. [1] Cholesterol serves critical roles in enveloped virus fusion by modulating membrane properties. [2]胆固醇通过调节膜特性在包膜病毒融合中发挥关键作用。 [1] 胆固醇通过调节膜特性在包膜病毒融合中发挥关键作用。 [2]
virus fusion protein
Importantly, the tip of domain II is structurally conserved between the alphavirus and flavivirus fusion proteins, yet whether these structural similarities between virus families translate to functional similarities is unclear. [1] In the second example, we review our studies of a parainfluenza virus fusion protein that merges the cell membrane and the virus envelope during virus entry. [2] In this review, we summarize some of the basic NMR structure based approaches and techniques which aid in improving the activity of AMPs, using the example of a 16-residue dengue virus fusion protein derived peptide, VG16KRKP. [3] Introduction The study objective was to characterize the excretion and metabolic profile of the respiratory syncytial virus fusion protein inhibitor, JNJ-53718678. [4] Here, we analyzed protease digestion products of a coronavirus fusion protein during activation; their sizes appear to be affected directly by the conformational state. [5] Collectively, these results have implications for the refolding of pneumovirus and paramyxovirus fusion proteins and should inform development of prefusion-stabilized RSV F vaccine candidates. [6] We report here the X-ray structures of the syn1 and syn2 transmembrane subunit ectodomains, featuring a 6-helix bundle (6HB) typical of the post-fusion state of gamma-retrovirus and filovirus fusion proteins. [7] However, recent breakthroughs in the recombinant expression and stabilization of pneumovirus fusion proteins have facilitated in-depth characterization of antibody responses and structural epitopes, and have provided an enormous diversity of new monoclonal antibody candidates for therapeutic development. [8]重要的是，结构域 II 的末端在甲病毒和黄病毒融合蛋白之间是结构保守的，但病毒家族之间的这些结构相似性是否转化为功能相似性尚不清楚。 [1] 在第二个例子中，我们回顾了我们对副流感病毒融合蛋白的研究，该融合蛋白在病毒进入过程中融合了细胞膜和病毒包膜。 [2] 在这篇综述中，我们以 16 残基登革热病毒融合蛋白衍生肽 VG16KRKP 为例，总结了一些基于 NMR 结构的基本方法和技术，这些方法和技术有助于提高 AMP 的活性。 [3] 简介 本研究的目的是描述呼吸道合胞病毒融合蛋白抑制剂 JNJ-53718678 的排泄和代谢特征。 [4] 在这里，我们分析了一种冠状病毒融合蛋白在激活过程中的蛋白酶消化产物；它们的大小似乎直接受构象状态的影响。 [5] 总的来说，这些结果对肺病毒和副粘病毒融合蛋白的重新折叠具有重要意义，并应为融合前稳定的 RSV F 候选疫苗的开发提供信息。 [6] 我们在此报告 syn1 和 syn2 跨膜亚基胞外域的 X 射线结构，具有典型的 γ-逆转录病毒和丝状病毒融合蛋白的融合后状态的 6 螺旋束 (6HB)。 [7] 然而，最近在肺病毒融合蛋白的重组表达和稳定化方面取得的突破促进了对抗体反应和结构表位的深入表征，并为治疗开发提供了大量新的候选单克隆抗体。 [8]
virus fusion inhibitor 病毒融合抑制剂
Here, we report on the antiviral activity and pre-clinical development of the novel broad-spectrum arenavirus fusion inhibitors, ARN-75039 and ARN-75041. [1] Out of 17 peptides, Fp13 and Fp14 showed better binding affinity toward HR1 compared to a control peptide EK1 (a modified pan-coronavirus fusion inhibitor) in molecular docking. [2] Inhibition of SARS-CoV-2 (previously 2019-nCoV) infection by a highly potent pan-coronavirus fusion inhibitor targeting its spike protein that harbors a high capacity to mediate membrane fusion. [3] Furthermore, ITZ shows broad‐spectrum activity targeting 6‐HB in the S2 subunit of SARS‐CoV and MERS‐CoV S protein, inspiring that ITZ have the potential for development as a pan‐coronavirus fusion inhibitor. [4] This study facilitates the potential repurposing of isavuconazole for therapeutic intervention against human-pathogenic arenaviruses, and provides the basis for further structural optimization of arenavirus fusion inhibitors based on the predicted structural characteristics of the unique SSP-GP2 interface. [5] EK1 is a broad-spectrum human coronavirus fusion inhibitor for combating infection of current and emerging coronaviruses. [6] 5]decan‐4‐yl)‐carboxamide compounds carrying the 5‐chloro‐2‐methoxybenzamide structure, designed as influenza virus fusion inhibitors. [7] Compound 8n and structural analogs were devoid of anti‐influenza virus activity, although their scaffold is shared with a previously discovered class of H3 hemagglutinin‐specific influenza virus fusion inhibitors. [8]在这里，我们报告了新型广谱沙粒病毒融合抑制剂 ARN-75039 和 ARN-75041 的抗病毒活性和临床前发展。 [1] 在 17 种肽中，与对照肽 EK1（一种修饰的泛冠状病毒融合抑制剂）相比，Fp13 和 Fp14 在分子对接中显示出对 HR1 更好的结合亲和力。 [2] 通过一种高效的泛冠状病毒融合抑制剂抑制 SARS-CoV-2（以前的 2019-nCoV）感染，该抑制剂靶向其具有高介导膜融合能力的刺突蛋白。 [3] 此外，ITZ 显示出针对 SARS-CoV S2 亚基中的 6-HB 和 MERS-CoV S 蛋白的广谱活性，这激发了 ITZ 作为泛冠状病毒融合抑制剂的发展潜力。 [4] 该研究有助于将艾沙康唑重新用于治疗干预人类致病性沙粒病毒，并基于独特的 SSP-GP2 界面的预测结构特征为沙粒病毒融合抑制剂的进一步结构优化提供基础。 [5] EK1 是一种广谱人类冠状病毒融合抑制剂，用于对抗当前和新兴冠状病毒的感染。 [6] 5]癸-4-基)-甲酰胺化合物，具有5-氯-2-甲氧基苯甲酰胺结构，设计为流感病毒融合抑制剂。 [7] 化合物 8n 和结构类似物缺乏抗流感病毒活性，尽管它们的支架与先前发现的一类 H3 血凝素特异性流感病毒融合抑制剂共享。 [8]
virus fusion peptide
We propose a 2-step mechanism for the interaction of the dengue virus fusion peptide with the host membrane, where the N-terminal sequence docks electrostatically on the headgroups and then the C-terminal interacts via hydrophobic forces in the acyl chains. [1] In the present study, we investigate the mechanism of interaction of VG16KRKP (VARGWKRKCPLFGKGG), a novel AMP designed from the dengue-virus fusion peptide, with bacterial/fungal membrane mimics. [2] This study shows that calcium directly targets the Ebola virus fusion peptide and influences its conformation. [3]我们提出了登革病毒融合肽与宿主膜相互作用的两步机制，其中 N 端序列静电停靠在头部基团上，然后 C 端通过酰基链中的疏水力相互作用。 [1] 在本研究中，我们研究了 VG16KRKP (VARGWKRKCPLFGKGG) 的相互作用机制，这是一种由登革热病毒融合肽设计的新型 AMP，与细菌/真菌膜模拟物的相互作用。 [2] 这项研究表明，钙直接靶向埃博拉病毒融合肽并影响其构象。 [3]
virus fusion study 病毒融合研究
Single-virus fusion studies to elucidate the dynamics of content mixing typically require extensive fluorescent labeling of viral contents. [1] Single-virus fusion studies to elucidate the dynamics of content mixing typically require extensive fluorescent labeling of viral contents. [2]阐明内容混合动态的单病毒融合研究通常需要对病毒内容物进行广泛的荧光标记。 [1] 阐明内容混合动态的单病毒融合研究通常需要对病毒内容物进行广泛的荧光标记。 [2]