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限制融合蛋白mRNA作为麻疹病毒持续存在的一种机制。

Restriction of fusion protein mRNA as a mechanism of measles virus persistence.

作者信息

Hummel K B, Vanchiere J A, Bellini W J

机构信息

Respiratory and Enterovirus Branch, Centers for Disease Control and Prevention, Atlanta, Georgia 30333.

出版信息

Virology. 1994 Aug 1;202(2):665-72. doi: 10.1006/viro.1994.1388.

DOI:10.1006/viro.1994.1388
PMID:8030232
Abstract

Vero cells persistently infected with the hamster neurotropic strain (HNT-PI) of measles virus are deficient in the release of extracellular virus and syncytia formation, suggesting that mutations occur within the viral envelope proteins. Nucleotide sequence comparisons indicated that the coding regions of the matrix (M) and fusion (F) genes of HNT-PI were relatively conserved compared with those of their lytic progenitor virus Philadelphia 26 (Ph26), whereas the hemagglutinin (H) gene differed by 4.2% at the amino acid level. Northern blot analyses demonstrated the predominance of bicistronic M/F transcripts in HNT-PI at a 5:1 ratio over F monocistronic mRNA. Accordingly, no F protein could be detected in the HNT-PI cell line, although both the M and H proteins were produced in amounts comparable to those of Ph26. When the Semliki Forest virus replicon was used, coexpression of the HNT-PI F and Ph26 H genes resulted in the formation of multinucleated syncytia in transfected Vero cell cultures. Since the HNT-PI F protein was fusogenic, the restriction of its monocistronic mRNA is postulated to be a contributing factor in the reduction of cell fusion and ultimately in the maintenance of the persistent infection.

摘要

持续感染麻疹病毒仓鼠嗜神经毒株(HNT-PI)的非洲绿猴肾细胞(Vero细胞)在细胞外病毒释放和多核巨细胞形成方面存在缺陷,这表明病毒包膜蛋白发生了突变。核苷酸序列比较表明,与溶细胞性亲代病毒费城26株(Ph26)相比,HNT-PI的基质(M)基因和融合(F)基因的编码区相对保守,而血凝素(H)基因在氨基酸水平上有4.2%的差异。Northern印迹分析表明,在HNT-PI中,双顺反子M/F转录本以5:1的比例占主导地位,高于F单顺反子mRNA。因此,在HNT-PI细胞系中未检测到F蛋白,尽管M蛋白和H蛋白的产生量与Ph26相当。当使用辛德毕斯病毒复制子时,HNT-PI F基因和Ph26 H基因的共表达导致转染的Vero细胞培养物中形成多核巨细胞。由于HNT-PI F蛋白具有融合活性,推测其单顺反子mRNA的限制是细胞融合减少以及最终维持持续感染的一个促成因素。

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