With no limiting membrane surrounding virions, nonenveloped viruses have no need for membrane fusion to gain access to intracellular replication compartments. Consequently, nonenveloped viruses do not encode membrane fusion proteins. The only exception to this dogma is the fusogenic reoviruses that encode fusion-associated small transmembrane (FAST) proteins that induce syncytium formation. FAST proteins are the smallest viral membrane fusion proteins and, unlike their enveloped virus counterparts, are nonstructural proteins that evolved specifically to induce cell-to-cell, not virus-cell, membrane fusion. This distinct evolutionary imperative is reflected in structural and functional features that distinguish this singular family of viral fusogens from all other protein fusogens. These rudimentary fusogens comprise specific combinations of different membrane effector motifs assembled into small, modular membrane fusogens. FAST proteins offer a minimalist model to better understand the ubiquitous process of protein-mediated membrane fusion and to reveal novel mechanisms of nonenveloped virus dissemination that contribute to virulence.

中文翻译：

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融合性呼肠孤病毒及其融合相关小跨膜（FAST）蛋白。

由于没有围绕病毒粒子的限制性膜，非包膜病毒无需进行膜融合即可进入细胞内复制区室。因此，非包膜病毒不编码膜融合蛋白。该教条的唯一例外是融合呼肠孤病毒，其编码诱导融合体形成的融合相关小跨膜（FAST）蛋白。FAST蛋白是最小的病毒膜融合蛋白，与它们的包膜病毒对应物不同，FAST蛋白是非结构蛋白，专门进化以诱导细胞间（而非病毒细胞）膜融合。这种独特的进化势力在结构和功能特征上得到了体现，这些特征将病毒融合蛋白的这一奇异家族与所有其他蛋白质融合蛋白区分开来。这些基本的融合剂包括组装成小的模块化薄膜融合剂的不同膜效应子基序的特定组合。FAST蛋白提供了一个极简主义的模型，可以更好地了解蛋白介导的膜融合的普遍过程，并揭示无包膜病毒传播的新机制，这种机制有助于提高毒性。