Lipids and proteins act in opposing manners to regulate polyomavirus infection.
Lipids and proteins act in opposing manners to regulate polyomavirus infection.
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脂质和蛋白质以相反的方式作用来调节多瘤病毒感染。
DOI：
10.1128/jvi.01093-10
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发表时间：
2010
影响因子：
5.4
通讯作者：
Tsai,Billy
中科院分区：
文献类型：
--
作者：
Qian,Mengding;Tsai,Billy
受体如何控制病毒感染还知之甚少。多瘤病毒（Py）与受体上的唾液酸-半乳糖部分结合以进入宿主细胞并引起感染。我们以前证明，含有唾液酸半乳糖的糖脂称为神经节苷脂GD 1a和GT 1b促进Py感染，部分是通过将病毒从内溶酶体分选到内质网（ER），这是一个关键的感染途径。然而，这些糖脂是否充当Py进入受体尚不清楚。此外，由于大多数糖蛋白也含有末端唾液酸-半乳糖残基，因此它们在Py感染中的作用也没有很好地确定。使用神经节苷脂缺陷的细胞系，我们表明，GD 1a是Py的功能进入受体。GD 1a与质膜上的Py结合，受体-病毒复合物被内化并转运到晚期内体，然后转运到ER以启动感染。相反，我们的研究结果表明，糖蛋白作为诱饵受体，限制ER运输和感染的Py。因此，糖脂和糖蛋白，质膜的两种主要成分，在调节特定病毒的感染中执行相反的功能。
How receptors control virus infection is poorly understood. Polyomavirus (Py) binds to the sialic acid-galactose moiety on receptors to gain entry into host cells and cause infection. We previously demonstrated that the sialic acid-galactose-containing glycolipids called gangliosides GD1a and GT1b promote Py infection, in part, by sorting the virus from the endolysosomes to the endoplasmic reticulum (ER), a critical infection route. Whether these glycolipids act as Py entry receptors, however, is not clear. Additionally, as the majority of glycoproteins also harbor terminal sialic acid-galactose residues, their roles in Py infection are also not well established. Using a ganglioside-deficient cell line, we show that GD1a is the functional entry receptor for Py. GD1a binds to Py on the plasma membrane, and the receptor-virus complex is internalized and transported to the late endosomes and then the ER to initiate infection. In contrast, our findings indicate that glycoproteins act as decoy receptors, restricting the ER transport and infection of Py. Thus, glycolipids and glycoproteins, two major constituents of the plasma membrane, execute opposing functions in regulating infection by a defined virus.