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病毒在室管膜和脉络丛上皮细胞中的不对称出芽。

Asymmetric budding of viruses in ependymal and choroid plexus epithelial cells.

作者信息

Kristensson K, Lundh B, Norrby E, Payne L, Orvell C

出版信息

Neuropathol Appl Neurobiol. 1984 May-Jun;10(3):209-19. doi: 10.1111/j.1365-2990.1984.tb00352.x.

Abstract

Sendai virus injected intracerebrally into 3-week-old mice caused infection of ependymal and choroid plexus epithelial cells. Budding of mature viruses occurred only from the apical surfaces of these cells. The viral peplomere proteins, haemagglutinin-neuraminidase and fusion, were concentrated on the apical portion of the ependymal cells, while the nucleocapsid-associated polymerase protein was dispersed throughout the cytoplasm. This indicates that intracellular routing of the virus envelope glycoproteins to the cell surface may be one of the factors that determines the site of virus budding. Vesicular stomatitis and vaccinia viruses, on the other hand, budded or egressed predominantly from the baso-lateral cell surfaces.

摘要

将仙台病毒脑内注射到3周龄小鼠体内,可导致室管膜和脉络丛上皮细胞感染。成熟病毒仅从这些细胞的顶端表面出芽。病毒包膜糖蛋白血凝素-神经氨酸酶和融合蛋白集中在室管膜细胞的顶端部分,而核衣壳相关的聚合酶蛋白则分散在整个细胞质中。这表明病毒包膜糖蛋白向细胞表面的细胞内运输可能是决定病毒出芽部位的因素之一。另一方面,水泡性口炎病毒和痘苗病毒主要从细胞基底外侧表面出芽或释放。

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