Binding of sindbis virus to cell surface heparan sulfate

Binding of sindbis virus to cell surface heparan sulfate
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DOI:
10.1128/jvi.72.9.7349-7356.1998
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发表时间:
1998-09-01
影响因子:
5.4
通讯作者:
Griffin, DE
Griffin, DE
中科院分区:
医学2区
文献类型:
--
作者:
Brynes, AP;Griffin, DE

文献摘要

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甲病毒是节肢动物传播的病毒,具有广泛的物种范围和不同的组织嗜性。允许如此多的不同物种和细胞类型的感染的细胞表面受体仍然不完全特征化。我们在这里表明,广泛表达的糖胺聚糖硫酸乙酰肝素可以参与辛德毕斯病毒与细胞的结合。酶法去除硫酸乙酰肝素或使用硫酸乙酰肝素缺陷细胞导致病毒结合大幅减少。辛德毕斯病毒结合固定肝素,这种相互作用被阻断的中和抗体对病毒E2糖蛋白。进一步的实验表明,高度硫酸化对于肝素结合辛德毕斯病毒的能力至关重要。然而,辛德毕斯病毒仍然能够感染硫酸乙酰肝素完全缺乏的细胞并在其上复制,这表明必须涉及额外的受体。发现另一种甲病毒Ross River病毒的细胞表面结合不依赖于硫酸乙酰肝素。
Alphaviruses are arthropod-borne viruses with wide species ranges and diverse tissue tropisms. The cell surface receptors which allow infection of so many different species and cell types are still incompletely characterized. We show here that the,widely expressed glycosaminoglycan heparan sulfate can participate in the binding of Sindbis virus to cells. Enzymatic removal of heparan sulfate or the use of heparan sulfate-deficient cells led to a large reduction in virus binding. Sindbis virus bound to immobilized heparin, and this interaction was blocked by neutralizing antibodies against the viral E2 glycoprotein. Further experiments showed that a high degree of sulfation was critical for the ability of heparin to bind Sindbis virus. However, Sindbis virus was still able to infect and replicate on cells which were completely deficient in heparan sulfate, indicating that additional receptors must be involved. Cell surface binding of another alphavirus, Ross River virus, was found to be independent of heparan sulfate.