Gain or loss of diabetogenicity resulting from a single point mutation in recombinant encephalomyocarditis virus
Gain or loss of diabetogenicity resulting from a single point mutation in recombinant encephalomyocarditis virus
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DOI：
10.1128/jvi.71.12.9782-9785.1997
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发表时间：
1997-12-01
影响因子：
5.4
通讯作者：
Yoon, JW
中科院分区：
文献类型：
--
作者：
Jun, HS;Kang, Y;Yoon, JW
病毒引起疾病的分子致病机制已受到相当大的关注。脑心肌炎(EMC)病毒诱导的小鼠糖尿病已被广泛研究，以阐明该病发生发展的细胞和分子机制。在这项研究中，我们首次报道了位于主要衣壳蛋白VP1上的重组EMC病毒基因组3155或3156位核苷酸的单点突变，导致氨基酸变化，导致病毒非致突变性的增强或丧失。位于核苷酸位置3155的G碱基(EMC病毒多蛋白[Ala(776)]；的776位氨基酸的丙氨酸)导致病毒的糖尿病致性，而同一或下一个位置的其他碱基的替代导致病毒糖尿病致病性的丧失。这一发现提供了明确的证据，表明病毒基因组关键位置的点突变会影响病毒引起细胞特异性疾病的能力。
Molecular pathogenic mechanisms for virus-induced disease have received considerable attention. Encephalomyocarditis (EMC) virus-induced diabetes in mice has been extensively studied to elucidate the cellular and molecular mechanisms involved in the development of this disease. In this study, we report for the first time that a single point mutation at nucleotide position 3155 or 3156 of the recombinant EMC viral genome, located on the major capsid protein VP1, which causes an amino acid change, results in the gain or loss of viral diabetogenicity. A G base at nucleotide position 3155 (alanine at amino acid position 776 of the EMC virus polyprotein [Ala(776)]; ) results in viral diabetogenicity, whereas the substitution of other bases at the same or next position results in a loss of viral diabetogenicity. This finding provides clear evidence that a point mutation at a critical site in a viral genome affects the ability of the virus to cause a cell-specific disease.