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将一段28S核糖体RNA序列插入流感病毒血凝素基因后病毒致病性增强。

Increased viral pathogenicity after insertion of a 28S ribosomal RNA sequence into the haemagglutinin gene of an influenza virus.

作者信息

Khatchikian D, Orlich M, Rott R

机构信息

Institut für Virologie, Justus-Liebig-Universität Giessen, FRG.

出版信息

Nature. 1989 Jul 13;340(6229):156-7. doi: 10.1038/340156a0.

Abstract

The haemagglutinin glycoprotein HA of influenza viruses is responsible for the attachment of the virus to neuraminic acid-containing receptors at the cell surface and subsequent penetration by triggering fusion of the viral envelope with cellular membranes. To express full activity of the newly synthesized precursor, HA has to be modified by post-translational proteolytic cleavage into the polypeptides HA1 and HA2 by cellular enzymes. If proteases suitable for cleavage are not present in the host cell, the resulting virus particles are non-infectious. During adaptation of the apathogenic influenza virus A/turkey/Oregon/71 to chicken embryo cells, which are not permissive for HA cleavage, we obtained an infectious virus variant with increased pathogenicity. Sequence analysis revealed that during adaptation 54 nucleotides were inserted into the HA gene; their sequence corresponds to a region of the 28S ribosomal RNA. This insertion is probably responsible for increased cleavability of HA, as well as for infectivity and pathogenicity of the adapted virus.

摘要

流感病毒的血凝素糖蛋白HA负责病毒与细胞表面含神经氨酸受体的结合,并通过触发病毒包膜与细胞膜融合实现后续侵入。为表达新合成前体的全部活性,HA必须经细胞酶进行翻译后蛋白水解切割,形成多肽HA1和HA2。如果宿主细胞中不存在适合切割的蛋白酶,产生的病毒颗粒将无感染性。在将无致病性的甲型流感病毒A/火鸡/俄勒冈/71适应鸡胚细胞(对HA切割不敏感)的过程中,我们获得了一种致病性增强的感染性病毒变体。序列分析显示,适应过程中HA基因插入了54个核苷酸;其序列与28S核糖体RNA的一个区域相对应。这种插入可能是HA切割性增强以及适应病毒的感染性和致病性增加的原因。

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