Salinas Yessenia, Roux Laurent
Department of Microbiology and Molecular Medicine, University of Geneva Medical School, CMU, 1 rue Michel-Servet, CH-1211 Geneva 4, Switzerland.
Virus Res. 2005 May;109(2):125-32. doi: 10.1016/j.virusres.2004.11.015. Epub 2004 Dec 10.
In the course of a Sendai virus infection, short genome versions (called defective) are frequently produced. These compete with the full length genome for replication (hence called interfering) and decrease the severity of the infection. The portion of the defective genome required for this effect can be limited, much shorter than the size of the defective genome. We postulated then that defective genome size follows from conditions required for their production more than for exerting the protective effect. Therefore, we set up experiments to determine which of the steps involved in their production may require this larger size. We constructed a series of Sendai virus mini-genomes, increasing their size from the smallest possible and we followed their ability to replicate, to amplify through multiples cycles of infection and to be packaged into virus particles, all steps required for their efficient production. We found that the mini-genomes replicated and amplified efficiently regardless of their size. The uptake into virus particles, however, depended on a threshold length. The data suggest no limitation in the ability of the viral RNA polymerase to generate and amplify very short size defective genomes. They however, point to limitations in the ability of short genomes to be packaged into virus particles.
在仙台病毒感染过程中,经常会产生短基因组版本(称为缺陷型)。这些缺陷型基因组与全长基因组竞争复制(因此称为干扰型),并降低感染的严重程度。产生这种效应所需的缺陷型基因组部分可能是有限的,比缺陷型基因组的大小短得多。于是我们推测,缺陷型基因组的大小更多地取决于其产生所需的条件,而非发挥保护作用所需的条件。因此,我们开展实验以确定其产生过程中的哪些步骤可能需要更大的尺寸。我们构建了一系列仙台病毒微型基因组,从尽可能小的尺寸开始增加其大小,并观察它们的复制能力、通过多个感染周期进行扩增的能力以及被包装进病毒颗粒的能力,这些都是其高效产生所必需的步骤。我们发现,微型基因组无论大小都能高效复制和扩增。然而,进入病毒颗粒则取决于一个阈值长度。数据表明,病毒RNA聚合酶生成和扩增非常短的缺陷型基因组的能力没有限制。然而,这些数据指出了短基因组被包装进病毒颗粒的能力存在限制。