Department of Pediatrics, University of Rochester School of Medicine and Dentistry, Medical Center, 601 Elmwood Avenue, Rochester, NY 14642, USA.
J Virol. 2010 Nov;84(21):10946-55. doi: 10.1128/JVI.00229-10. Epub 2010 Jul 28.
Experiments in the 1960s showed that Sendai virus, a paramyxovirus, fused its membrane with the host plasma membrane. After membrane fusion, the virus spontaneously "uncoated" with diffusion of the viral membrane proteins into the host plasma membrane and a merging of the host and viral membranes. This led to deposit of the viral ribonucleoprotein (RNP) and interior proteins in the cell cytoplasm. Later work showed that the common procedure then used to grow Sendai virus produced damaged, pleomorphic virions. Virions, which were grown under conditions that were not damaging, made a connecting structure between virus and cell at the region where the fusion occurred. The virus did not release its membrane proteins into the host membrane. The viral RNP was seen in the connecting structure in some cases. Uncoating of intact Sendai virus proceeds differently from uncoating described by the current standard model developed long ago with damaged virus. A model of intact paramyxovirus uncoating is presented and compared to what is known about the uncoating of other viruses.
20 世纪 60 年代的实验表明,副粘病毒仙台病毒会将其膜与宿主质膜融合。膜融合后,病毒会自发地“脱壳”,病毒膜蛋白扩散到宿主质膜中,宿主和病毒的膜融合。这导致病毒核糖核蛋白(RNP)和内部蛋白在细胞质中沉积。后来的研究表明,当时常用的生长仙台病毒的方法会产生受损的、多形的病毒粒子。在不具破坏性的条件下生长的病毒粒子,会在融合发生的区域形成病毒与细胞之间的连接结构。病毒不会将其膜蛋白释放到宿主膜中。在某些情况下,可以在连接结构中看到病毒的 RNP。完整仙台病毒的脱壳过程与很久以前用受损病毒建立的现行标准模型所描述的脱壳过程不同。本文提出了一种完整副粘病毒脱壳模型,并将其与其他病毒脱壳的已知情况进行了比较。