欧博电脑版下载:Nature:A型血或诱发轮状病毒传染

新2备用网址/2020-06-29/ 分类:财经/阅读:

一小我私人是否被轮状病毒传染也许抉择于他的血型。一些轮状病毒通过辨认与A型血相干的抗原本找到进入胃肠道细胞的途径,这一颁发于Nature上的研究发明,给相识肠道病原体怎样传染人类描画了一种新模式。

肠道内病原体--轮状病毒是一种首要的肠道病原体,是全天下婴儿严峻脱水与腹泻的首要缘故起因。据预计,全天下每有50万人死于传染。已知的P[14]是病毒株要害部门的布局,这提供了病毒怎样传染人细胞的一条线索。在传染动物的轮状病毒中,病毒上穗状顶部经一个具唾液酸结尾分子的聚糖(很多毗连在一路形成伟大分枝链布局的糖之一)吸附到细胞上。在传染人的真实病毒株上没有呈现沟通情形,研究职员以为人轮状病毒通过内涵唾液酸分子与聚糖团结,可是不知道这是怎样产生的。

惊人发明--各人想知道的是这种轮状病毒遗传型怎样辨认细胞内聚糖,与VP8*彼此浸染的只有一种聚糖,即构造血型抗原A,这很让人惊奇,由于我们一向以为病毒是与具唾液酸聚糖彼此浸染,而构造血型抗原A无唾液酸。研究职员还发明,A型聚糖在与动物轮状病毒唾液酸沟通的位置团结轮状病毒穗状卵白。已知构造血型抗原促进诺如病毒和幽门螺旋杆菌细胞与肠道细胞的团结,但这在轮状病毒中一向没有被证实。

VP8*域--结晶学研究表白,病毒VP8*域布局的渺小变革可使病毒将构造血型抗体原A作为受体来用。尝试室表达构造血型抗原A的改善细胞很轻易被这种轮状病毒株传染,缺乏这种抗原的细胞则不轻易被传染。构造血型抗原A抗体能阻断病毒对作育人肠道细胞的传染。更深入的研究判断出了第二种轮状病毒株P[9],它也将构造血型抗原看成受体用。

新撒播机制--上面研究很紧张,由于它们提供了轮状病毒从有蹄动物(如马、斑马、猪、羊)跳跃至人的一种新撒播机制。研究发明,传染P[14]株的人是A型血,血型与病毒传染间是否存在关联还必要更多研究才气证明。(生物谷bioon.com)

doi:10.1038/nature10996
PMC:
PMID:

Cell attachment protein VP8* of a human rotavirus specifically interacts with A-type histo-blood group antigen

Liya Hu, Sue E. Crawford, Rita Czako, Nicolas W. Cortes-Penfield, David F. Smith, Jacques Le Pendu, Mary K. Estes & B. V. Venkataram Prasad

As with many other viruses, the initial cell attachment of rotaviruses, which are the major causative agent of infantile gastroenteritis, is mediated by interactions with specific cellular glycans1, 2, 3, 4. The distally located VP8* domain of the rotavirus spike protein VP4 (ref. 5) mediates such interactions. The existing paradigm is that 'sialidase-sensitive' animal rotavirus strains bind to glycans with terminal sialic acid (Sia), whereas 'sialidase-insensitive' human rotavirus strains bind to glycans with internal Sia such as GM1 (ref. 3). Although the involvement of Sia in the animal strains is firmly supported by crystallographic studies1, 3, 6, 7, it is not yet known how VP8* of human rotaviruses interacts with Sia and whether their cell attachment necessarily involves sialoglycans. Here we show that VP8* of a human rotavirus strain specifically recognizes A-type histo-blood group antigen (HBGA) using a glycan array screen comprised of 511 glycans, and that virus infectivity in HT-29 cells is abrogated by anti-A-type antibodies as well as significantly enhanced in Chinese hamster ovary cells genetically modified to express the A-type HBGA, providing a novel paradigm for initial cell attachment of human rotavirus. HBGAs are genetically determined glycoconjugates present in mucosal secretions, epithelia and on red blood cells8, and are recognized as susceptibility and cell attachment factors for gastric pathogens like Helicobacter pylori9 and noroviruses10. Our crystallographic studies show that the A-type HBGA binds to the human rotavirus VP8* at the same location as the Sia in the VP8* of animal rotavirus, and suggest how subtle changes within the same structural framework allow for such receptor switching. These results raise the possibility that host susceptibility to specific human rotavirus strains and pathogenesis are influenced by genetically controlled expression of different HBGAs among the world's population.

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