E2包膜糖蛋白胞质结构域突变对辛德毕斯病毒发病机制的影响。
Effect of E2 envelope glycoprotein cytoplasmic domain mutations on Sindbis virus pathogenesis.
作者信息
Levine B, Jiang H H, Kleeman L, Yang G
机构信息
Department of Medicine, Columbia University College of Physicians & Surgeons, New York, New York 10032, USA.
出版信息
J Virol. 1996 Feb;70(2):1255-60. doi: 10.1128/JVI.70.2.1255-1260.1996.
Abstract
The cytoplasmic domain of the E2 envelope glycoprotein is important in Sindbis virus assembly, but little is known about its role in the pathogenesis of Sindbis virus encephalitis. To investigate its role in viral pathogenesis, we constructed six recombinant viruses containing site mutations in the E2 cytoplasmic domain, using the neurovirulent background strain, TE12. Our findings demonstrate that the E2 cytoplasmic domain is a determinant of Sindbis virus growth and neurovirulence in suckling mice as well as persistent infection in weanling scid mice. They also suggest that the tyrosine, serine, or threonine residues are not essential for replication in mouse brain or anti-E2 monoclonal antibody-mediated restriction of Sindbis virus replication.
摘要
E2包膜糖蛋白的细胞质结构域在辛德毕斯病毒组装过程中很重要，但对其在辛德毕斯病毒脑炎发病机制中的作用知之甚少。为了研究其在病毒发病机制中的作用，我们使用神经毒力背景毒株TE12构建了六种在E2细胞质结构域含有位点突变的重组病毒。我们的研究结果表明，E2细胞质结构域是辛德毕斯病毒在乳鼠中的生长和神经毒力以及在断奶scid小鼠中持续感染的决定因素。这些结果还表明，酪氨酸、丝氨酸或苏氨酸残基对于在小鼠脑中的复制或抗E2单克隆抗体介导的辛德毕斯病毒复制限制并非必不可少。
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