The Dual Role of TRIM7 in Viral Infections

Viruses Pub Date : 2024-08-12 DOI:10.3390/v16081285
Maria Gonzalez-Orozco, Carlos A. Rodriguez-Salazar, Maria I. Giraldo
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Abstract

The E3 ubiquitin ligase TRIM7 is known to have dual roles during viral infections. Like other TRIM proteins, TRIM7 can regulate the IFN pathway via the regulation of the cytosolic receptors RIG-I or MDA-5, which promote the production of type I interferons (IFN-I) and antiviral immune responses. Alternatively, under certain infectious conditions, TRIM7 can negatively regulate IFN-I signaling, resulting in increased virus replication. A growing body of evidence has also shown that TRIM7 can, in some cases, ubiquitinate viral proteins to promote viral replication and pathogenesis, while in other cases it can promote degradation of viral proteins through the proteasome, reducing virus infection. TRIM7 can also regulate the host inflammatory response and modulate the production of inflammatory cytokines, which can lead to detrimental inflammation. TRIM7 can also protect the host during infection by reducing cellular apoptosis. Here, we discuss the multiple functions of TRIM7 during viral infections and its potential as a therapeutic target.
TRIM7 在病毒感染中的双重作用
已知E3泛素连接酶TRIM7在病毒感染过程中具有双重作用。与其他 TRIM 蛋白一样,TRIM7 可通过调节细胞膜受体 RIG-I 或 MDA-5 来调节 IFN 通路,从而促进 I 型干扰素(IFN-I)的产生和抗病毒免疫反应。另外,在某些感染条件下,TRIM7 还能负向调节 IFN-I 信号传导,导致病毒复制增加。越来越多的证据还表明,在某些情况下,TRIM7 可以泛素化病毒蛋白,促进病毒复制和致病,而在其他情况下,它可以通过蛋白酶体促进病毒蛋白降解,减少病毒感染。TRIM7 还能调节宿主的炎症反应,调节炎症细胞因子的产生,从而导致有害的炎症。TRIM7 还能在感染期间通过减少细胞凋亡来保护宿主。在此,我们将讨论 TRIM7 在病毒感染过程中的多种功能及其作为治疗靶点的潜力。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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