Study on the Pathogenesis of Dengue Hepatitis

Wenli Li, Qian Wang, Fangfang Wei, Eying Lu, Yunzhi Ling, Mao-sheng Wu
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引用次数: 0

Abstract

Dengue virus (DENV) is a single-stranded RNA virus that is transmitted by Aedes aegypti and Aedes albopictus. As a global health problem, early diagnosis and timely treatment of DENV are imperative. Therefore, it is important to explore the association between dengue fever and hepatitis and its pathogenesis and development mechanism of action. This may lead to the identification of biological markers for the prevention and treatment of dengue fever-induced hepatitis. In this study, we identified differentially expressed genes associated with interferon signaling to further understand the relationship between dengue fever and hepatitis. It has been speculated that during dengue-induced hepatitis, DEXD/H-box helicase 58 (DDX58) and interferon-induced protein with tetratricopeptide repeats 1 (IFIT1) are primarily responsible for pathogen identification. The joint action of HECT and RLD domain containing E3 ubiquitin protein ligase 5 (HERC5) and ubiquitinspecific peptidase 18 (USP18) regulate the biological effects of interferon and participate in the occurrence and development of this disease.
登革肝炎发病机制的研究
登革热病毒(DENV)是一种单链RNA病毒,由埃及伊蚊和白纹伊蚊传播。作为一个全球性的卫生问题,DENV的早期诊断和及时治疗至关重要。因此,探讨登革热与肝炎的关系及其发病机制和发展作用机制具有重要意义。这可能导致识别预防和治疗登革热引起的肝炎的生物标志物。在这项研究中,我们鉴定了与干扰素信号相关的差异表达基因,以进一步了解登革热和肝炎之间的关系。据推测,在登革热诱导的肝炎中,DEXD/H-box解旋酶58 (DDX58)和干扰素诱导的四肽重复1蛋白(IFIT1)主要负责病原体识别。HECT与含有E3泛素蛋白连接酶5 (HERC5)和泛素特异性肽酶18 (USP18)的RLD结构域共同作用,调节干扰素的生物学效应,参与本病的发生发展。
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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来源期刊
Nanoscience and Nanotechnology Letters
Nanoscience and Nanotechnology Letters Physical, Chemical & Earth Sciences-MATERIALS SCIENCE, MULTIDISCIPLINARY
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审稿时长
2.6 months
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