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SAMD9L抑制了弗拉维病毒的翻译,而不依赖于它触发天生的免疫反应的能力

Marion Cannac^1,2, Jim Zoladek¹, Inès Bribes¹

¹Institut de Recherche en Infectiologie de Montpellier (IRIM), Univ Montpellier, CNRS UMR9004, INSERM, Montpellier, France.

|December 8, 2025

概括

人类SAMD9类蛋白 (SAMD9L) 作为广泛的抗病毒因子,通过抑制病毒转化来限制寨卡和登革热等危险黄病毒的复制. 这确定SAMD9L是髓状细胞中关键的先天免疫防御.

科学领域:

天生的免疫力和病毒学.
细胞的抗病毒机制.
在宿主-病原体相互作用中的基因调节.

背景情况:

干扰素刺激基因 (ISG) 对先天性抗病毒反应至关重要.
SAMD9和SAMD9L是具有已知的转化抑制抗病毒活性的ISG.
SAMD9L限制了晶状病毒,但它对其他病毒家族的作用不太清楚.

研究的目的:

调查SAMD9和SAMD9L对医学相关的黄病毒的抗病毒活性.
为了阐明SAMD9L介导的黄病毒限制的机制.
为了确定SAMD9L在原发性免疫细胞中在黄病毒感染期间的作用.

主要方法:

在人类细胞中,SAMD9/SAMD9L的外源表达和敲除.
病毒复制测试用于西尼罗河病毒,寨卡病毒,登革热病毒和乌苏图病毒.
对病毒RNA翻译和先天免疫激活标记物的分析.
研究人类骨髓状细胞,包括微质细胞和原发性巨细胞.

主要成果:

SAMD9L,但不是SAMD9,强烈抑制了多个黄病毒的复制.
SAMD9L knockdown 损害了I型干扰素在髓状细胞中的抗病毒活性.
SAMD9L通过抑制病毒RNA通过其核糖酶域的翻译来限制flavivirus的复制.
SAMD9L的抗病毒活性独立于先天免疫激活.

结论:

人类SAMD9L是一种广泛的限制因子,对医学上重要的黄状病毒.
SAMD9L通过抑制flaviviralRNA转化而起作用,独立于一般免疫激活.
SAMD9L是髓状细胞中的关键抗病毒ISG,对抗黄病毒的天生的防御至关重要.

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