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首页> 外文期刊>Infectious disorders drug targets >Insights into Ebola Virus VP35 and VP24 Interferon Inhibitory Functions and their Initial Exploitation as Drug Targets
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Insights into Ebola Virus VP35 and VP24 Interferon Inhibitory Functions and their Initial Exploitation as Drug Targets

机译：埃博拉病毒VP35和VP24干扰素抑制功能及其作为药物靶点的初步开发

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摘要

Upon viral infection, the interferon (IFN) system triggers potent antiviral mechanisms limiting viral growth and spread. Hence, to sustain their infection, viruses evolved efficient counteracting strategies to evade IFN control. Ebola virus (EBOV), member of the family Filoviridae, is one of the most virulent and deadly pathogen ever faced by humans. The etiological agent of the Ebola Virus Disease (EVD), EBOV can be undoubtedly considered the perfect example of a powerful inhibitor of the host organism immune response activation. Particularly, the efficacious suppression of the IFN cascade contributes to disease progression and severity. Among the EBOV-encoded proteins, the Viral Proteins 35 (VP35) and 24 (VP24) are responsible for the EBOV extreme virulence, representing the core of such inhibitory function through which EBOV determines its very effective shield to the cellular immune defenses. VP35 inhibits the activation of the cascade leading to IFN production, while VP24 inhibits the activation of the IFN-stimulated genes. A number of studies demonstrated that both VP35 and VP24 is validated target for drug development. Insights into the structural characteristics of VP35 and VP24 domains revealed crucial pockets exploitable for drug development. Considered the lack of therapy for EVD, restoring the immune activation is a promising approach for drug development. In the present review, we summarize the importance of VP35 and VP24 proteins in counteracting the host IFN cellular response and discuss their potential as druggable viral targets as a promising approach toward attenuation of EBOV virulence.
机译：病毒感染后，干扰素 （IFN） 系统会触发有效的抗病毒机制，限制病毒的生长和传播。因此，为了维持感染，病毒进化出有效的对抗策略来逃避IFN控制。埃博拉病毒（EBOV）是丝状病毒科的成员，是人类有史以来最致命和最致命的病原体之一。埃博拉病毒病（EVD）的病原体EBOV无疑可以被认为是宿主生物体免疫反应激活的强大抑制剂的完美例子。特别是，IFN级联反应的有效抑制有助于疾病的进展和严重程度。在EBOV编码的蛋白质中，病毒蛋白35（VP35）和24（VP24）负责EBOV的极端毒力，代表了这种抑制功能的核心，EBOV通过该抑制功能决定了其对细胞免疫防御的非常有效的屏蔽。VP35 抑制导致 IFN 产生的级联反应的激活，而 VP24 抑制 IFN 刺激基因的激活。多项研究表明，VP35 和 VP24 都是经验证的药物开发靶点。对 VP35 和 VP24 结构域结构特征的深入了解揭示了可用于药物开发的关键口袋。考虑到缺乏对埃博拉病毒病的治疗，恢复免疫激活是一种很有前途的药物开发方法。在本综述中，我们总结了 VP35 和 VP24 蛋白在抵消宿主 IFN 细胞反应中的重要性，并讨论了它们作为可成药病毒靶标作为减弱 EBOV 毒力的有前途的方法的潜力。

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