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Updated: Jun 13, 2025

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在感染期间,SLC35A2调节了paramyxovirus融合事件

Yanling Yang¹, Yuchen Wang¹, Danielle E Campbell²

¹Department of Molecular Microbiology and Center for Women Infectious Disease Research, Washington University School of Medicine, St. Louis, MO, USA.

bioRxiv : the preprint server for biology

|September 10, 2024

概括

新的研究确定了关键宿主因素,CMP-酸载体 (CST) 和UDP-银糖载体 (UGT),对于帕拉米克索病毒感染至关重要,影响病毒的进入和传播.

科学领域:

病毒学病毒学
分子生物学分子生物学
细胞生物学细胞生物学

背景情况:

帕拉米克索病毒,包括疹病毒 (MuV),纽卡斯尔病病毒 (NDV) 和仙台病毒 (SeV),是人类和动物的重要病原体.
关于宿主因子控制帕拉米克索病毒感染的知识仍然有限,阻碍了治疗的发展.

研究的目的:

通过功能丧失CRISPR屏幕识别对帕拉米克索病毒感染至关重要的新宿主因素.
阐明确定宿主因子在帕拉米克索病毒进入,融合和传播中的特定作用.

主要方法:

一种表达不稳定的GFP (rSeVC^dseGFP) 的重组仙台病毒 (SeV) 被用于全基因组的CRISPR功能丧失屏幕.
针对已识别的基因 (SLC35A1和SLC35A2) 的淘汰 (KO) 细胞系被生成并分析病毒结合,进入和融合效率.
评估病毒结合细胞的形成,以评估细胞间的传播.

主要成果:

鉴定出CMP-酸载体 (CST) 基因SLC35A1和UDP-银糖载体 (UGT) 基因SLC35A2对于帕拉米克索病毒感染至关重要.
由于缺少已知病毒受体的酸,KO细胞表现出减少SeV,NDV和MuV的结合和感染.
SLC35A2 KO 细胞揭示了 UGT 在病毒-细胞和细胞-细胞融合中的关键作用,对 SeV,NDV 和 MuV 进入和突触形成的差异性要求.

结论:

帕拉米克索病毒可以感染缺乏正规酸受体的细胞,突出显示了其他进入机制.
UDP-银河糖转运体 (UGT) 在促进病毒进入和细胞间传播期间的帕拉米克索病毒融合事件中发挥着至关重要的作用.
这些发现提供了对宿主-病原体相互作用的新见解,以及对抗paramyxoviruses的抗病毒策略的潜在目标.

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