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肠道黏蛋白以寡糖依赖的方式抑制轮状病毒复制。

Intestinal mucins inhibit rotavirus replication in an oligosaccharide-dependent manner.

作者信息

Yolken R H, Ojeh C, Khatri I A, Sajjan U, Forstner J F

机构信息

Department of Pediatric Infectious Diseases, Johns Hopkins University School of Medicine, Baltimore, Maryland.

出版信息

J Infect Dis. 1994 May;169(5):1002-6. doi: 10.1093/infdis/169.5.1002.

Abstract

Rotaviruses are important causes of infant morbidity and mortality worldwide. It has been previously shown that mucinous glycoproteins can inhibit rotavirus replication. However, the structure-function relationships of this inhibition have not been completely elucidated. Mucins were purified from epithelial scrapings of rat and human intestine by CsCl density-gradient ultracentrifugation and tested for the inhibition of rotavirus replication in MA-104 cells. Native human and rat intestinal mucins inhibited the replication of human and animal rotaviruses at low concentrations. Antiviral activity was most prominent in the densely glycosylated part of the rat and human mucins. Activity was retained after thiol reduction and alkylation, chloroform methanol partition, and partial removal of oligosaccharides. However, total deglycosylation of the mucins destroyed antiviral activity. Intestinal mucins from humans and other animals are potent inhibitors of rotavirus replication, and this inhibition is dependent on specific mucin-viral interactions.

摘要

轮状病毒是全球范围内婴儿发病和死亡的重要原因。先前已经表明,黏液糖蛋白可以抑制轮状病毒复制。然而,这种抑制作用的结构-功能关系尚未完全阐明。通过氯化铯密度梯度超速离心从大鼠和人类肠道的上皮刮屑中纯化黏蛋白,并检测其对MA-104细胞中轮状病毒复制的抑制作用。天然的人类和大鼠肠道黏蛋白在低浓度下就能抑制人类和动物轮状病毒的复制。抗病毒活性在大鼠和人类黏蛋白的高度糖基化部分最为显著。在巯基还原和烷基化、氯仿-甲醇分配以及部分去除寡糖后,活性仍然保留。然而,黏蛋白的完全去糖基化会破坏抗病毒活性。人类和其他动物的肠道黏蛋白是轮状病毒复制的有效抑制剂,并且这种抑制作用依赖于特定的黏蛋白-病毒相互作用。

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