宿主脂滴的上调驱动抗病毒反应。

IF 4.1 Q2 CELL BIOLOGY
Cell Stress Pub Date : 2021-08-25 eCollection Date: 2021-09-01 DOI:10.15698/cst2021.09.256
Ebony A Monson, Karla J Helbig
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引用次数: 4

摘要

当宿主细胞被病毒感染时,它会激活先天免疫反应,引发一系列信号事件,导致抗病毒反应的产生。这种免疫反应通常是强大的,通常可以很好地清除病毒感染,然而,病毒已经进化出逃避策略来对抗这种感染,因此,需要更好地了解这种反应是如何更详细地起作用的,以便开发新的有效的治疗方法。脂滴(ld)是细胞内细胞器,历史上一直被认为是细胞能量来源,然而,最近被认为是信号传导事件中的关键细胞器。重要的是,已知许多病毒接管宿主细胞的ld生产,传统上认为其唯一目的是为病毒生命周期事件提供能量。然而,我们最近的研究表明,在抗病毒反应的最初几个小时内,ld是重要的细胞器,表明它们支持病毒感染后重要抗病毒细胞因子的产生。在细胞被RNA病毒(寨卡病毒、登革热病毒、甲型流感病毒)或DNA病毒(单纯疱疹病毒-1)感染后,ld迅速上调,这种反应在病毒模拟激动剂刺激后也被复制。感染后LDs的上调是短暂的,有趣的是,它并没有遵循目前所描述的LD上调的稳态机制,而是由EGFR控制的。当抑制EGFR时,细胞产生有效免疫反应的能力大大降低,从而抑制了感染期间LD的上调,也导致病毒复制的增加。在这篇微观综述中,我们推断了我们最近的发现,并讨论了ld作为先天免疫反应中的重要细胞器。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Host upregulation of lipid droplets drives antiviral responses.

Host upregulation of lipid droplets drives antiviral responses.

When a host cell is infected by a virus, it activates the innate immune response, setting off a cascade of signalling events leading to the production of an antiviral response. This immune response is typically robust and in general works well to clear viral infections, however, viruses have evolved evasion strategies to combat this, and therefore, a better understanding of how this response works in more detail is needed for the development of novel and effective therapeutics. Lipid droplets (LDs) are intracellular organelles and have historically been thought of simply as cellular energy sources, however, have more recently been recognised as critical organelles in signalling events. Importantly, many viruses are known to take over host cellular production of LDs, and it has traditionally been assumed the sole purpose of this is to supply energy for viral life cycle events. However, our recent work positions LDs as important organelles during the first few hours of an antiviral response, showing that they underpin the production of important antiviral cytokines following viral infection. Following infection of cells with either RNA viruses (Zika, Dengue, Influenza A) or a DNA (Herpes Simplex Virus-1) virus, LDs were rapidly upregulated, and this response was also replicated following stimulation with viral mimic agonists. This upregulation of LDs following infection was transient, and interestingly, did not follow the well described homeostatic mechanism of LD upregulation, instead being controlled by EGFR. The cell's ability to mount an effective immune response was greatly diminished when inhibiting EGFR, thus inhibiting LD upregulation during infection, also leading to an increase in viral replication. In this microreview, we extrapolate our recent findings and discuss LDs as an important organelle in the innate immune response.

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来源期刊
Cell Stress
Cell Stress Biochemistry, Genetics and Molecular Biology-Biochemistry, Genetics and Molecular Biology (miscellaneous)
CiteScore
13.50
自引率
0.00%
发文量
21
审稿时长
15 weeks
期刊介绍: Cell Stress is an open-access, peer-reviewed journal that is dedicated to publishing highly relevant research in the field of cellular pathology. The journal focuses on advancing our understanding of the molecular, mechanistic, phenotypic, and other critical aspects that underpin cellular dysfunction and disease. It specifically aims to foster cell biology research that is applicable to a range of significant human diseases, including neurodegenerative disorders, myopathies, mitochondriopathies, infectious diseases, cancer, and pathological aging. The scope of Cell Stress is broad, welcoming submissions that represent a spectrum of research from fundamental to translational and clinical studies. The journal is a valuable resource for scientists, educators, and policymakers worldwide, as well as for any individual with an interest in cellular pathology. It serves as a platform for the dissemination of research findings that are instrumental in the investigation, classification, diagnosis, and therapeutic management of major diseases. By being open-access, Cell Stress ensures that its content is freely available to a global audience, thereby promoting international scientific collaboration and accelerating the exchange of knowledge within the research community.
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