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神经毒力流感病毒株A/NWS/33血凝素基因的变化

Changes in the hemagglutinin gene of the neurovirulent influenza virus strain A/NWS/33.

作者信息

Ward A C, de Koning-Ward T F

机构信息

Biomolecular Research Institute, Parkville, Victoria, Australia.

出版信息

Virus Genes. 1995;10(2):179-83. doi: 10.1007/BF01702599.

DOI:10.1007/BF01702599
PMID:8560778
Abstract

The neurovirulent strain of influenza A virus, A/NWS/33, is able to infect a large range of cell types, including mouse brain cells, which are not infected by its parent, A/WS/33. This seems to be largely due to the hemagglutinin of A/NWS/33. The complete nucleotide sequence of the HA genes of both strains has been determined and a comparison revealed a number of changes. Analysis showed that the virulence capabilities of the NWS HA involve at least three different mechanisms: (a) loss of a glycosylation site; (b) a change at the cleavage site; and (c) a substitution in HA2, which may increase the pH of fusion.

摘要

甲型流感病毒的神经毒株A/NWS/33能够感染多种细胞类型,包括小鼠脑细胞,而其亲代毒株A/WS/33则不能感染这些细胞。这似乎主要归因于A/NWS/33的血凝素。已确定了这两种毒株HA基因的完整核苷酸序列,比较结果显示存在一些变化。分析表明,NWS HA的致病能力至少涉及三种不同机制:(a)一个糖基化位点的缺失;(b)裂解位点的变化;以及(c)HA2中的一个替代,这可能会提高融合的pH值。

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