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MFSD6是D68肠道病毒的入口受体

Lauren Varanese¹, Lily Xu¹, Christine E Peters¹

¹Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA, USA.

|March 25, 2025

概括

研究人员确定MFSD6是D68肠道病毒 (EV-D68) 的关键宿主进入因子,这种病毒会引起急性软骨髓炎. 针对MFSD6提供了对抗这种新出现的病原体的潜在策略.

科学领域:

病毒学和分子生物学
神经科学与传染病

背景情况:

全球疫苗接种减少了脊髓灰质炎病毒,重点转移到其他引起急性软骨炎 (AFM) 的肠道病毒.
肠道病毒D68 (EV-D68) 是最近的AFM爆发的主要原因,但其宿主相互作用仍然不明.
EV-D68是一种呼吸道病毒,可引起严重的中枢神经系统疾病.

研究的目的:

确定参与EV-D68进入和感染的宿主因素.
阐明EV-D68与宿主细胞相互作用的分子机制.
探索EV-D68感染的潜在治疗点.

主要方法:

用基因组规模的CRISPR选来确定EV-D68的宿主因子.
在CRISPR查中,MFSD6被确定为关键宿主进入因子.
使用冷电子显微镜来确定EV-D68-MFSD6相互作用的结构基础.

主要成果:

在呼吸和神经细胞类型中,MFSD6淘汰消除了EV- D68感染.
MFSD6是病毒进入所必需的血蛋白,通过细胞外环3直接与EV- D68结合.
针对MFSD6 L3的诱受体阻断了EV-D68的感染并保护了致命感染模型中的小鼠.

结论:

MFSD6充当了EV-D68的特定进入受体.
在结构上描述了MFSD6 L3和EV- D68之间的相互作用接口.
针对MFSD6是一种有前途的治疗策略,可以对抗EV-D68感染和潜在的未来疫情.

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