PDF(Pubmed)
Abstract：
Over the past few years, the attention of the whole world has been riveted to the emergence of new dangerous strains of viruses, among which a special place is occupied by coronaviruses that have overcome the interspecies barrier in the past 20 years: SARS viruses (SARS), Middle East respiratory syndrome (MERS), as well as a new coronavirus infection (SARS-CoV-2), which caused the largest pandemic since the Spanish flu in 1918. Coronaviruses are members of a class of enveloped viruses that have a lipoprotein envelope. This class also includes such serious pathogens as human immunodeficiency virus (HIV), hepatitis, Ebola virus, influenza, etc. Despite significant differences in the clinical picture of the course of disease caused by enveloped viruses, they themselves have a number of characteristic features, which determine their commonality. Regardless of the way of penetration into the cell-by endocytosis or direct fusion with the cell membrane-enveloped viruses are characterized by the following stages of interaction with the target cell: binding to receptors on the cell surface, interaction of the surface glycoproteins of the virus with the membrane structures of the infected cell, fusion of the lipid envelope of the virion with plasma or endosomal membrane, destruction of the protein capsid and its dissociation from the viral nucleoprotein. Subsequently, within the infected cell, the newly synthesized viral proteins must self-assemble on various membrane structures to form a progeny virion. Thus, both the initial stages of viral infection and the assembly and release of new viral particles are associated with the activity of viral proteins in relation to the cell membrane and its organelles. This review is devoted to the analysis of physicochemical mechanisms of functioning of the main structural proteins of a number of enveloped viruses in order to identify possible strategies for the membrane activity of such proteins at various stages of viral infection of the cell.
摘要：
在过去的几年里，全世界的注意力都集中在新的危险病毒株的出现上，其中一个特殊的地方是在过去20年中克服了种间障碍的冠状病毒：SARS病毒（SARS），中东呼吸综合征（MERS）以及新的冠状病毒感染（SARS-CoV-2），这是自1918年西班牙流感以来最大的一次大流行。冠状病毒是一类具有脂蛋白包膜的包膜病毒的成员。此类还包括人类免疫缺陷病毒（HIV）等严重病原体，肝炎，埃博拉病毒,流感,等。尽管由包膜病毒引起的病程的临床表现存在显着差异，它们本身具有许多特征，这决定了它们的共性。无论通过内吞作用或与细胞膜包膜病毒直接融合进入细胞的方式如何，其特征在于与靶细胞相互作用的以下阶段：与细胞表面的受体结合，病毒的表面糖蛋白与被感染细胞的膜结构相互作用，病毒粒子的脂质包膜与血浆或内体膜融合，蛋白质衣壳的破坏及其与病毒核蛋白的解离。随后，在被感染的细胞内，新合成的病毒蛋白必须在各种膜结构上自组装才能形成子代病毒体。因此，病毒感染的初始阶段以及新病毒颗粒的组装和释放都与病毒蛋白相对于细胞膜及其细胞器的活性有关。这篇综述致力于分析许多包膜病毒的主要结构蛋白的功能的物理化学机制，以确定在病毒感染细胞的各个阶段此类蛋白的膜活性的可能策略。
