小鼠冠状病毒株A59和JHM的复制酶基因可互换：发病机制的差异定位于基因组的3'端三分之一处。
Replicase genes of murine coronavirus strains A59 and JHM are interchangeable: differences in pathogenesis map to the 3' one-third of the genome.
作者信息
Navas-Martin Sonia, Brom Maarten, Chua Ming-Ming, Watson Richard, Qiu Zhaozhu, Weiss Susan R
机构信息
Department of Microbiology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA.
出版信息
J Virol. 2007 Jan;81(2):1022-6. doi: 10.1128/JVI.01944-06. Epub 2006 Nov 1.
Abstract
The important roles of the spike protein and other structural proteins in murine coronavirus (MHV) pathogenesis have been demonstrated; however, the role of the replicase gene remains unexplored. We assessed the influence of the replicase genes of the highly neurovirulent MHV-JHM strain and the hepatotropic and mildly neurovirulent A59 strain in acute infection of the mouse. Analysis of chimeric A59/JHM recombinant viruses indicates that the replicase genes are interchangeable and that it is the 3' end of the genome, encoding the structural proteins, rather than the replicase gene, that determines the pathogenic properties of these chimeras.
摘要
刺突蛋白和其他结构蛋白在鼠冠状病毒（MHV）发病机制中的重要作用已得到证实；然而，复制酶基因的作用仍未得到探索。我们评估了高神经毒力的MHV-JHM株和嗜肝性及轻度神经毒力的A59株的复制酶基因在小鼠急性感染中的影响。对嵌合A59/JHM重组病毒的分析表明，复制酶基因是可互换的，并且是基因组的3'端，即编码结构蛋白的部分，而非复制酶基因，决定了这些嵌合体的致病特性。
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