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[金刚烷类抗病毒制剂的作用分子机制]

[The molecular mechanism of the action of antiviral preparations in the adamantane series].

作者信息

Kiselev O I, Blinov V M, Kozeletskaia K N, Il'enko V I, Platonov V G, Chupakhin O N, Stukova M A, Karginov V A

出版信息

Vestn Ross Akad Med Nauk. 1993(3):10-5.

PMID:7687902
Abstract

Regions of possible interaction between remantadine and transmembrane M2 protein are revealed by analysis of amino acid substitutions in remantadine- and deutiforin-resistant influenza viruses. The major region includes 5-6 amino acid residues at position 25-31, partially involving the premembrane region and the first position of a hydrophobic membrane-associated domain. The proposed model action of remantadine and its derivatives suggests that remantadine is included into the cell membrane lipid bimolecular layer by its adamantane share and its positively charged NH2-group is exposed to the cell surface. This allows remantadine and its analog to be regarded as molecular "hindrances" for viral particle decapsidation and budding.

摘要

通过对金刚乙胺和地替福林耐药流感病毒中氨基酸取代的分析,揭示了金刚乙胺与跨膜M2蛋白之间可能的相互作用区域。主要区域包括25 - 31位的5 - 6个氨基酸残基,部分涉及前膜区域和疏水膜相关结构域的第一个位置。所提出的金刚乙胺及其衍生物的作用模型表明,金刚乙胺通过其金刚烷部分被纳入细胞膜脂质双分子层,其带正电荷的NH2基团暴露于细胞表面。这使得金刚乙胺及其类似物可被视为病毒颗粒脱壳和出芽的分子“阻碍物”。

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