An Antiviral Role for TRIM14 in Ebola Virus Infection.
An Antiviral Role for TRIM14 in Ebola Virus Infection.
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TRIM14 在埃博拉病毒感染中的抗病毒作用。
DOI：
10.1093/infdis/jiad325
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发表时间：
2023
期刊：
影响因子：
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通讯作者：
Kawaoka,Yoshihiro
中科院分区：
文献类型：
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作者：
Kuroda,Makoto;Halfmann,PeterJ;Thackray,LarissaB;Diamond,MichaelS;Feldmann,Heinz;Marzi,Andrea;Kawaoka,Yoshihiro
埃博拉病毒（Ebola virus，EBOV）是一种高致病性病毒，编码7种多功能结构蛋白。已经报道了多种宿主因子与EBOV蛋白相互作用。在这里，我们发现，TRIM 14，一个干扰素刺激的基因，介导与I型干扰素和炎性细胞因子产生相关的细胞信号转导途径，与EBOV核蛋白相互作用，以增强干扰素-β（IFN-β）和核因子-κB（NF-κB）启动子的激活。此外，TRIM 14过表达使感染性但生物学上包含的EBOVΔ VP 30系统中的病毒复制减少约10倍，而不影响病毒蛋白表达。此外，TRM 14缺陷型小鼠比野生型小鼠更容易受到小鼠适应性EBOV感染。我们的数据表明TRIM 14是具有抗EBOV活性的宿主因子，其限制EBOV发病机制。
Ebola virus (EBOV) is a highly pathogenic virus that encodes 7 multifunctional structural proteins. Multiple host factors have been reported to interact with the EBOV proteins. Here, we found that tripartite motif-containing 14 (TRIM14), an interferon-stimulated gene that mediates cellular signaling pathways associated with type I interferon and inflammatory cytokine production, interacts with EBOV nucleoprotein to enhance interferon-β (IFN-β) and nuclear factor-κB (NF-κB) promotor activation. Moreover, TRIM14 overexpression reduced viral replication in an infectious but biologically contained EBOVΔVP30 system by approximately 10-fold without affecting viral protein expression. Furthermore, TRM14-deficient mice were more susceptible to mouse-adapted EBOV infection than wild-type mice. Our data suggest that TRIM14 is a host factor with anti-EBOV activity that limits EBOV pathogenesis.