Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555, USA.
Molecular Biology and Virology Laboratory, Faculty of Medicine and Health Sciences, Corporación Universitaria Empresarial Alexander von Humboldt, Armenia 630003, Colombia.
Viruses. 2024 Aug 12;16(8):1285. doi: 10.3390/v16081285.
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.
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 可以通过调节细胞质受体 RIG-I 或 MDA-5 来调节 IFN 途径，从而促进 I 型干扰素（IFN-I）的产生和抗病毒免疫反应。或者，在某些感染条件下，TRIM7 可以负调控 IFN-I 信号转导，导致病毒复制增加。越来越多的证据表明，TRIM7 可以在某些情况下泛素化病毒蛋白以促进病毒复制和发病机制，而在其他情况下，它可以通过蛋白酶体促进病毒蛋白的降解，从而减少病毒感染。TRIM7 还可以调节宿主炎症反应并调节炎症细胞因子的产生，这可能导致有害的炎症。TRIM7 还可以通过减少细胞凋亡来保护宿主免受感染。在这里，我们讨论了 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。
