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坦基拉酶通过I型干扰素反应积极调节流感A病毒的复制

Gayan Bamunuarachchi^1,2, Kishore Vaddadi^1,2, Yurong Liang^1,2

¹Oklahoma Center for Respiratory and Infectious Diseases, Oklahoma State University, Stillwater, Oklahoma, USA.

Journal of virology

|October 2, 2025

概括

坦基酶1和2 (TNKS1/2) 是促进流感A病毒 (IAV) 复制的宿主因素. 在细胞和小鼠中淘汰TNKS1/2可降低病毒载量并增加存活率,突出显示它们是潜在的抗病毒标.

科学领域:

病毒学病毒学
分子生物学分子生物学
免疫学免疫学免疫学

背景情况:

由于耐药性和流行病潜力,A型流感病毒 (IAV) 构成重大威胁.
目前的抗病毒药物向病毒蛋白质,但主体向策略正在出现.
多 (ADP-ribose) 聚合酶 (PARP) 是参与细胞过程的宿主因素,在IAV感染中没有明确的作用.

研究的目的:

选所有17个PARP成员在IAV复制中的作用.
为了确定可以针对针对IAV的新型抗病毒疗法的宿主因素.
调查确定PARP影响IAV感染的机制.

主要方法:

在肺上皮细胞A549细胞中对17个PARP成员进行CRISPR激活选.
在HEK293T细胞中,CRISPR-Cas9基因对Tankyrase 1和2 (TNKS1/2) 的淘汰.
在体外对病毒复制标记物 (mRNA,蛋白质,病毒标位) 的评估.
对宿主信号通路 (JNK/c-Jun,Stat) 和I型干扰素反应的分析.
在体内使用Tnks1/2淘汰赛小鼠的研究中,IAV.被挑战.

主要成果:

坦基拉斯1和2 (TNKS1/2) 被确定为IAV的强有力的前病毒因素.
TNKS1/2淘汰赛在体外显著降低了病毒复制和标位,双重淘汰赛显示出更大的效果.
TNKS1/2淘汰赛增强了I型干扰素反应,并激活了JNK/c-Jun和Stat信号通路.
在IAV挑战后,Tnks1/2淘汰赛小鼠表现出减少的病毒载量,增加的I型干扰素反应和显著更高的存活率.

结论:

TNKS1和TNKS2是促进流感A病毒复制的关键宿主因素.
准TNKS1/2可以增强宿主I型干扰素的反应,从而减少病毒载量和增加存活率.
TNKS1/2代表了开发新型抗流感A病毒策略的有希望的治疗点.

关键词:

聚 (ADP-ribose) 聚合酶的聚 (ADP-ribose) 聚合酶是什么在TNKS1上.在TNKS2上.流感A型病毒感染者翻译后的修改翻译后的修改一种类型I干扰素的反应反应.

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