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仙台病毒的缺陷干扰颗粒调节受感染的BHK细胞表面的HN表达。

Defective interfering particles of Sendai virus modulate HN expression at the surface of infected BHK cells.

作者信息

Roux L, Waldvogel F A

出版信息

Virology. 1983 Oct 15;130(1):91-104. doi: 10.1016/0042-6822(83)90120-4.

Abstract

The expression of the Sendai viral glycoproteins HN and F0 at the surface of BHK 21 cells was studied during infection with standard virus, with a mixture of standard and defective interfering (DI) particles (mixed virus infection), and during persistent infection. It is shown that by 2 days after infection, the expression of the HN protein at the surface of mixed virus-infected cells is reduced compared to that observed on standard virus-infected cells as estimated by cell surface immune precipitation of iodinated proteins. This reduced expression results from a reduced efficiency of HN insertion in the plasma membrane, as well as from the inaccessibility to antibody of part of the HN present at the membrane. The HN protein is also poorly expressed at the surface of persistently infected cells, originally infected with a mixture of DI and standard virus particles. In contrast, the expression of the F0 protein at the surface of the infected cells is similar regardless of the type of infection.

摘要

在标准病毒感染、标准病毒与缺陷干扰(DI)颗粒混合感染(混合病毒感染)以及持续感染期间,研究了仙台病毒糖蛋白HN和F0在BHK 21细胞表面的表达情况。结果表明,感染后2天,通过碘化蛋白的细胞表面免疫沉淀估计,混合病毒感染细胞表面的HN蛋白表达与标准病毒感染细胞相比有所降低。这种表达降低是由于HN插入质膜的效率降低,以及膜上部分HN无法与抗体结合所致。HN蛋白在最初感染DI和标准病毒颗粒混合物的持续感染细胞表面的表达也很低。相比之下,无论感染类型如何,感染细胞表面的F0蛋白表达相似。

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