黄病毒包括大量的节肢动物病毒,其中一些与危及生命的疾病有关。黄病毒感染在全球范围内呈上升趋势,主要是由于其载体的扩散和地理扩展。人类主要病原体是蚊媒黄病毒,包括登革热病毒,寨卡病毒,和西尼罗河病毒,但是蜱传黄病毒也正在出现。和任何病毒感染一样,身体抵御黄病毒感染的第一道防线是先天免疫防御,其中I型干扰素是武装翼。这种细胞因子通过触发数百个干扰素诱导基因(ISG)的合成来发挥其抗病毒活性,其产品可以预防感染。在抑制黄病毒复制的ISG中,已经鉴定了某些三方基序(TRIM)蛋白。尽管参与了其他生物过程,TRIM构成了对多种病毒有活性的抗病毒蛋白的大家族。此外,而一些TRIM蛋白直接阻断病毒复制,其他人是IFN应答的正调节因子。因此,病毒已经开发出逃避或抵消TRIM蛋白的策略,有些甚至劫持某些TRIM蛋白以获取优势。在这次审查中,我们总结了黄病毒和TRIM蛋白之间相互作用的知识现状,涵盖直接和间接抗病毒机制。
Flaviviruses comprise a large number of arthropod-borne viruses, some of which are associated with life-threatening diseases. Flavivirus infections are rising worldwide, mainly due to the proliferation and geographical expansion of their vectors. The main human pathogens are mosquito-borne
flaviviruses, including dengue virus, Zika virus, and West Nile virus, but tick-borne
flaviviruses are also emerging. As with any viral infection, the body\'s first line of defense against flavivirus infections is the innate immune defense, of which type I interferon is the armed wing. This cytokine exerts its antiviral activity by triggering the synthesis of hundreds of interferon-induced genes (ISGs), whose products can prevent infection. Among the ISGs that inhibit flavivirus replication, certain tripartite motif (TRIM) proteins have been identified. Although involved in other biological processes, TRIMs constitute a large family of antiviral proteins active on a wide range of viruses. Furthermore, whereas some TRIM proteins directly block viral replication, others are positive regulators of the IFN response. Therefore, viruses have developed strategies to evade or counteract TRIM proteins, and some even hijack certain TRIM proteins to their advantage. In this review, we summarize the current state of knowledge on the interactions between
flaviviruses and TRIM proteins, covering both direct and indirect antiviral mechanisms.