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Phosphatidylserine treatment relieves the block to retrovirus infection of cells expressing glycosylated virus receptors

机译:磷脂酰丝氨酸治疗可缓解表达糖基化病毒受体的细胞对逆转录病毒感染的阻止

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Background A major determinant of retrovirus host range is the presence or absence of appropriate cell-surface receptors required for virus entry. Often orthologs of functional receptors are present in a wide range of species, but amino acid differences can render these receptors non-functional. In some cases amino acid differences result in additional N-linked glycosylation that blocks virus infection. The latter block to retrovirus infection can be overcome by treatment of cells with compounds such as tunicamycin, which prevent the addition of N-linked oligosaccharides. Results We have discovered that treatment of cells with liposomes composed of phosphatidylserine (PS) can also overcome the block to infection mediated by N-linked glycosylation. Importantly, this effect occurs without apparent change in the glycosylation state of the receptors for these viruses. This effect occurs with delayed kinetics compared to previous results showing enhancement of virus infection by PS treatment of cells expressing functional virus receptors. Conclusion We have demonstrated that PS treatment can relieve the block to retrovirus infection of cells expressing retroviral receptors that have been rendered non-functional by glycosylation. These findings have important implications for the current model describing inhibition of virus entry by receptor glycosylation.
机译:背景技术逆转录病毒宿主范围的主要决定因素是是否存在病毒进入所需的适当细胞表面受体。功能受体的直系同源物通常存在于各种各样的物种中,但是氨基酸差异会使这些受体失去功能。在某些情况下,氨基酸差异会导致额外的N-联糖基化,从而阻止病毒感染。逆转录病毒感染的后者阻滞可以通过用化合物(如衣霉素)处理细胞来克服,该化合物可以防止添加N-连接的寡糖。结果我们发现用磷脂酰丝氨酸(PS)组成的脂质体处理细胞也可以克服由N-联糖基化介导的感染阻滞。重要的是,在没有明显改变这些病毒的受体的糖基化状态的情况下发生了这种效应。与先前的结果相比,这种效应发生在动力学的延迟上,先前的结果表明通过PS处理表达功能性病毒受体的细胞可以增强病毒感染。结论我们已经证明PS疗法可以缓解表达由糖基化作用失效的表达逆转录病毒受体的细胞对逆转录病毒感染的阻滞。这些发现对描述受体糖基化抑制病毒进入的当前模型具有重要意义。

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