Recent work has identified three distinct classes of viral membrane fusion proteins based on structural criteria. In addition, there are at least four distinct mechanisms by which viral fusion proteins can be triggered to undergo fusion-inducing conformational changes. Viral fusion proteins also contain different types of fusion peptides and vary in their reliance on accessory proteins. These differing features combine to yield a rich diversity of fusion proteins. Yet despite this staggering diversity, all characterized viral fusion proteins convert from a fusion-competent state (dimers or trimers, depending on the class) to a membrane-embedded homotrimeric prehairpin, and then to a trimer-of-hairpins that brings the fusion peptide, attached to the target membrane, and the transmembrane domain, attached to the viral membrane, into close proximity thereby facilitating the union of viral and target membranes. During these conformational conversions, the fusion proteins induce membranes to progress through stages of close apposition, hemifusion, and then the formation of small, and finally large, fusion pores. Clearly, highly divergent proteins have converged on the same overall strategy to mediate fusion, an essential step in the life cycle of every enveloped virus.

中文翻译：

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病毒膜融合蛋白的结构和机制：共同主题的多种变化。

最近的工作已经根据结构标准确定了三类不同的病毒膜融合蛋白。此外，至少有四种不同的机制可以触发病毒融合蛋白进行融合诱导构象变化。病毒融合蛋白还包含不同类型的融合肽，它们对辅助蛋白的依赖程度各不相同。这些不同的特征相结合，产生了丰富多样的融合蛋白。然而，尽管存在这种惊人的多样性，所有特征化的病毒融合蛋白都从具有融合能力的状态（二聚体或三聚体，取决于类别）转变为膜嵌入的同源三聚体前发夹，然后转变为带有融合肽的发夹三聚体, 附着在靶膜上，以及跨膜域，附着在病毒膜上，靠近从而促进病毒和目标膜的结合。在这些构象转换过程中，融合蛋白诱导膜通过紧密并列、半融合、然后形成小的融合孔，最后形成大的融合孔。显然，高度不同的蛋白质已经集中在相同的整体策略上来介导融合，这是每个包膜病毒生命周期中必不可少的一步。