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膜活性剂对辛德毕斯病毒形态发生的影响。

The effect of membrane-active agents on Sindbis virus morphogenesis.

作者信息

Scupham R K, Sagik B P, Bose H R

出版信息

Intervirology. 1979;12(1):8-18. doi: 10.1159/000149063.

Abstract

In chicken cells infected by Sindbis virus and exposed to a variety of membrane-active compounds, virus release was inhibited. In infected cells exposed to antiserum directed against the virion glycoproteins E1 or E2, retinol, cortisone, Pb++ or insulin, the processing of two Sindbis virus precursor polypeptides which lead to the formation of virion polypeptides was inhibited. The B-protein, which is the precursor to both envelope proteins, accumulated in cells treated by these compounds. This precursor is generally not detected in chicken cells, presumably because it is processed rapidly. The cleavage of the precursor PE2 to the envelope glycoprotein E2 was also inhibited. E2 was also absent in cells exposed to menadione or to antiserum prepared against uninfected chicken cells. Since each of the compounds tested interfered with Sindbis virus polypeptide cleavage, despite their diverse mechanisms of action, it suggests that perturbation of normal membrane fluidity can interfere with Sindbis virus budding.

摘要

在被辛德毕斯病毒感染并暴露于多种膜活性化合物的鸡细胞中,病毒释放受到抑制。在暴露于针对病毒粒子糖蛋白E1或E2的抗血清、视黄醇、可的松、Pb++或胰岛素的感染细胞中,两种导致病毒粒子多肽形成的辛德毕斯病毒前体多肽的加工过程受到抑制。作为两种包膜蛋白前体的B蛋白在经这些化合物处理的细胞中积累。这种前体在鸡细胞中通常检测不到,大概是因为它被迅速加工。前体PE2裂解为包膜糖蛋白E2的过程也受到抑制。在暴露于甲萘醌或针对未感染鸡细胞制备的抗血清的细胞中也不存在E2。由于所测试的每种化合物都干扰了辛德毕斯病毒多肽的裂解,尽管它们的作用机制各不相同,但这表明正常膜流动性的扰动会干扰辛德毕斯病毒的出芽。

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