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轮状病毒株与细胞表面N-乙酰神经氨酸(唾液酸)残基的初始相互作用与VP4基因型相关,而非病毒的起源物种。

Initial interaction of rotavirus strains with N-acetylneuraminic (sialic) acid residues on the cell surface correlates with VP4 genotype, not species of origin.

作者信息

Ciarlet Max, Ludert Juan E, Iturriza-Gómara Miren, Liprandi Ferdinando, Gray James J, Desselberger Ulrich, Estes Mary K

机构信息

Department of Molecular Virology and Microbiology, Baylor College of Medicine, Houston, Texas 77030, USA.

出版信息

J Virol. 2002 Apr;76(8):4087-95. doi: 10.1128/jvi.76.8.4087-4095.2002.

Abstract

We examined 41 human and animal rotavirus strains representative of all known P genotypes for their dependency on cellular N-acetylneuraminic (sialic) acid (SA) residues for infectivity. Our results showed that all rotaviruses studied, whether of animal or human origin, belonging to P genotypes [1], [2], [3], and [7] depended on SA residues on the cell surface for efficient infectivity but that all human and animal rotavirus strains representative of the remaining known P genotypes were SA independent. The SA residue requirement for efficient infectivity did not change for reassortant rotavirus strains with altered VP4-VP7 combinations. The initial interaction of rotavirus strains with SA residues on the cell surface correlated with VP4 genotype specificity, not with species of origin or VP7 G serotype specificity (P = 0.001; r2 = 1.00, Pearson's correlation coefficient). In addition to being a requirement for infectivity, the presence of SA residues on the cell surface is a requirement for efficient growth in cell culture; recognition of the association of specific P genotypes with the binding of rotavirus to SA residues will facilitate our understanding of the molecular basis of the early events of rotavirus-cell interactions in cell culture models and of pathogenicity in vivo.

摘要

我们检测了41株代表所有已知P基因型的人源和动物源轮状病毒毒株,以研究其感染性对细胞N - 乙酰神经氨酸(唾液酸,SA)残基的依赖性。我们的结果表明,所有研究的轮状病毒,无论源自动物还是人类,属于P基因型[1]、[2]、[3]和[7]的毒株,其有效感染性均依赖于细胞表面的SA残基,但代表其余已知P基因型的所有人源和动物源轮状病毒毒株均不依赖SA。对于具有改变的VP4 - VP7组合的重配轮状病毒毒株,有效感染性对SA残基的需求并未改变。轮状病毒毒株与细胞表面SA残基的初始相互作用与VP4基因型特异性相关,而与病毒来源物种或VP7 G血清型特异性无关(P = 0.001;r2 = 1.00,皮尔逊相关系数)。细胞表面SA残基的存在不仅是感染性的必要条件,也是细胞培养中高效生长的必要条件;认识到特定P基因型与轮状病毒与SA残基结合之间的关联,将有助于我们理解细胞培养模型中轮状病毒 - 细胞相互作用早期事件的分子基础以及体内致病性。

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本文引用的文献

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Curr Opin Microbiol. 2001 Aug;4(4):435-41. doi: 10.1016/s1369-5274(00)00232-0.
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