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在日本大阪分离的亚急性硬化性全脑炎病毒株融合蛋白细胞质尾部的改变与多样性。

Alterations and diversity in the cytoplasmic tail of the fusion protein of subacute sclerosing panencephalitis virus strains isolated in Osaka, Japan.

作者信息

Ning Xiaojun, Ayata Minoru, Kimura Masatsugu, Komase Katsuhiro, Furukawa Kyoko, Seto Toshiyuki, Ito Nobuhisa, Shingai Masashi, Matsunaga Isamu, Yamano Tsunekazu, Ogura Hisashi

机构信息

Department of Virology, Osaka City University Medical School, Asahimachi, Abeno-ku, Osaka, Japan.

出版信息

Virus Res. 2002 Jun;86(1-2):123-31. doi: 10.1016/s0168-1702(02)00042-4.

Abstract

We determined the nucleotide sequence of the fusion (F) gene of three strains (Osaka-1, -2, and -3) of nonproductive variants of measles virus (MV). These viral strains were isolated in Osaka, Japan, from brain tissues of patients with subacute sclerosing panencephalitis (SSPE). Phylogenetic analysis revealed a close relationship among the three strains of SSPE virus. The cytoplasmic tail of the F protein, predicted from sequence analysis of the gene, is altered in all three SSPE strains when compared to the MV field strains. However, the extent and mode of alteration are different in each strain. The F protein of the Osaka-1 strain has six nonconservative amino acid substitutions and a 29-residue elongation of its cytoplasmic tail. The F protein of the Osaka-3 strain has two nonconservative substitutions and a 5-residue truncation of its C-terminus. Although the termination codon is not altered in the F protein of the Osaka-2 strain, five or six amino acids are changed in the cytoplasmic tail of the F protein of the two sibling viruses of this strain. The significance of the altered cytoplasmic domain of the SSPE viruses in the SSPE pathogenesis is discussed.

摘要

我们测定了麻疹病毒(MV)非生产性变异株的三个毒株(大阪-1、-2和-3)的融合(F)基因的核苷酸序列。这些病毒毒株是在日本大阪从亚急性硬化性全脑炎(SSPE)患者的脑组织中分离出来的。系统发育分析显示,这三株SSPE病毒之间关系密切。根据基因序列分析预测,与MV野毒株相比,所有三株SSPE毒株中F蛋白的胞质尾均发生了改变。然而,各毒株的改变程度和方式有所不同。大阪-1毒株的F蛋白有六个非保守氨基酸替换,其胞质尾延长了29个残基。大阪-3毒株的F蛋白有两个非保守替换,其C末端截短了5个残基。虽然大阪-2毒株的F蛋白中的终止密码子未改变,但该毒株的两个同源病毒的F蛋白的胞质尾中有五个或六个氨基酸发生了变化。文中讨论了SSPE病毒胞质结构域改变在SSPE发病机制中的意义。

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