DC-SIGN and DC-SIGNR interact with the glycoprotein of Marburg virus and the S protein of severe acute respiratory syndrome coronavirus
DC-SIGN and DC-SIGNR interact with the glycoprotein of Marburg virus and the S protein of severe acute respiratory syndrome coronavirus
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DOI：
10.1128/jvi.78.21.12090-12095.2004
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发表时间：
2004-11-01
影响因子：
5.4
通讯作者：
Pöhlmann, S
中科院分区：
文献类型：
--
作者：
Marzi, A;Gramberg, T;Pöhlmann, S
凝集素DC-SIGN和DC-SIGNR可以增强病毒感染;然而，与这些附着因子相互作用的病原体的范围尚未完全确定。我们发现DC-SIGN和DC-SIGNR增强了由马尔堡病毒（MARV）糖蛋白（GP）和严重急性呼吸综合征冠状病毒S蛋白介导的感染，并可能促进病毒传播。SIGNR 1是一种鼠DC-SIGN同源物，也增强了由MARV和埃博拉病毒GP驱动的感染，并且可以靶向评估附着因子在体内丝状病毒感染中的作用。
The lectins DC-SIGN and DC-SIGNR can augment viral infection; however, the range of pathogens interacting with these attachment factors is incompletely defined. Here we show that DC-SIGN and DC-SIGNR enhance infection mediated by the glycoprotein (GP) of Marburg virus (MARV) and the S protein of severe acute respiratory syndrome coronavirus and might promote viral dissemination. SIGNR1, a murine DC-SIGN homologue, also enhanced infection driven by MARV and Ebola virus GP and could be targeted to assess the role of attachment factors in filovirus infection in vivo.