A polymorphism of the TIM-1 IgV domain: implications for the susceptibility to filovirus infection.
A polymorphism of the TIM-1 IgV domain: implications for the susceptibility to filovirus infection.
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DOI：
10.1016/j.bbrc.2014.10.144
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发表时间：
2014-12-12
影响因子：
3.1
通讯作者：
Takada A
中科院分区：
文献类型：
--
作者：
Kuroda M;Fujikura D;Noyori O;Kajihara M;Maruyama J;Miyamoto H;Yoshida R;Takada A
在非洲绿色猴肾细胞系中比较TIM-1基因。Vero E6衍生的TIM-1具有增加的促进丝状病毒进入的潜力。IgV结构域主要参与TIM-1介导的丝状病毒进入。IgV结构域中的单个氨基酸对于TIM-1的能力增加至关重要。TIM-1基因多态性可能影响细胞对丝状病毒感染的易感性。丝状病毒，包括埃博拉病毒和马尔堡病毒，在人类和非人灵长类动物中引起严重的出血热，死亡率高达90%。人T细胞免疫球蛋白和粘蛋白结构域1（TIM-1）是已显示促进丝状病毒进入细胞的宿主蛋白之一。本研究从非洲绿色猴肾细胞系（Vero E6、COS-1和BSC-1）中克隆了TIM-1基因，发现与COS-1和BSC-1相比，Vero E6的TIM-1有23个氨基酸缺失和6个氨基酸替换。有趣的是，Vero E6 TIM-1比COS-1衍生的TIM-1具有更大的促进用丝状病毒糖蛋白假型化的水泡性口炎病毒的感染性的能力。我们进一步发现，Vero E6 TIM-1促进病毒感染性的能力增加很可能是由于这些TIM-1之间的单个氨基酸差异。这些结果表明，TIM-1分子的多态性是影响细胞对丝状病毒感染易感性的因素之一，为丝状病毒宿主范围的分子基础提供了新的见解。
TIM-1 genes were compared among African green monkey kidney cell lines. Vero E6-derived TIM-1 has increased potential to promote filovirus entry. The IgV domain is primarily involved in TIM-1-mediated filovirus entry. A single amino acid in the IgV domain is crucial for the increased ability of TIM-1. TIM-1 polymorphism may affect the cell susceptibility to filovirus infection. Filoviruses, including Ebola and Marburg viruses, cause severe hemorrhagic fever in humans and nonhuman primates with mortality rates of up to 90%. Human T-cell immunoglobulin and mucin domain 1 (TIM-1) is one of the host proteins that have been shown to promote filovirus entry into cells. In this study, we cloned TIM-1 genes from three different African green monkey kidney cell lines (Vero E6, COS-1, and BSC-1) and found that TIM-1 of Vero E6 had a 23-amino acid deletion and 6 amino acid substitutions compared with those of COS-1 and BSC-1. Interestingly, Vero E6 TIM-1 had a greater ability to promote the infectivity of vesicular stomatitis viruses pseudotyped with filovirus glycoproteins than COS-1-derived TIM-1. We further found that the increased ability of Vero E6 TIM-1 to promote virus infectivity was most likely due to a single amino acid difference between these TIM-1s. These results suggest that a polymorphism of the TIM-1 molecules is one of the factors that influence cell susceptibility to filovirus infection, providing a new insight into the molecular basis for the filovirus host range.
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