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呼吸道合胞病毒利用缺氧诱导因子-1α 介导的糖酵解作用促进感染性病毒的产生。

Respiratory syncytial virus co-opts hypoxia-inducible factor-1α-mediated glycolysis to favor the production of infectious virus.

机构信息

Department of Dermatology, The First Affiliated Hospital, Jinan University , Guangzhou, Guangdong, China.

Guangdong Province Key Laboratory of Pharmacodynamic Constituents of TCM and New Drugs Research, College of Pharmacy, Jinan University , Guangzhou, Guangdong, China.

出版信息

mBio. 2023 Oct 31;14(5):e0211023. doi: 10.1128/mbio.02110-23. Epub 2023 Oct 5.

DOI:10.1128/mbio.02110-23
PMID:37796013
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10653832/
Abstract

Respiratory syncytial virus (RSV) is the leading etiological agent of lower respiratory tract illness. However, efficacious vaccines or antiviral drugs for treating RSV infections are currently not available. Indeed, RSV depends on host cells to provide energy needed to produce progeny virions. Glycolysis is a series of oxidative reactions used to metabolize glucose and provide energy to host cells. Therefore, glycolysis may be helpful for RSV infection. In this study, we show that RSV increases glycolysis by inducing the stabilization, transcription, translation, and activation of hypoxia-inducible factor (HIF)-1α in infected cells, which is important for the production of progeny RSV virions. This study contributes to understanding the molecular mechanism by which HIF-1α-mediated glycolysis controls RSV infection and reveals an effective target for the development of highly efficient anti-RSV drugs.

摘要

呼吸道合胞病毒(RSV)是引起下呼吸道疾病的主要病原体。然而,目前尚无有效的疫苗或抗病毒药物可用于治疗 RSV 感染。事实上,RSV 依赖宿主细胞提供产生子代病毒所需的能量。糖酵解是一系列氧化反应,用于代谢葡萄糖并为宿主细胞提供能量。因此,糖酵解可能有助于 RSV 感染。在这项研究中,我们表明 RSV 通过诱导感染细胞中缺氧诱导因子(HIF)-1α的稳定、转录、翻译和激活来增加糖酵解,这对于产生子代 RSV 病毒粒子很重要。本研究有助于了解 HIF-1α 介导的糖酵解控制 RSV 感染的分子机制,并揭示了开发高效抗 RSV 药物的有效靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/947b/10653832/6913d81de619/mbio.02110-23.f009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/947b/10653832/4aea60b7fa70/mbio.02110-23.f001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/947b/10653832/0cf56fa7310a/mbio.02110-23.f005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/947b/10653832/829e9db468a5/mbio.02110-23.f006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/947b/10653832/579b87c50e4d/mbio.02110-23.f007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/947b/10653832/0e4edf5bc512/mbio.02110-23.f008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/947b/10653832/6913d81de619/mbio.02110-23.f009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/947b/10653832/4aea60b7fa70/mbio.02110-23.f001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/947b/10653832/8ed3311106b8/mbio.02110-23.f002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/947b/10653832/6d4f2677dfca/mbio.02110-23.f003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/947b/10653832/80c7e39ff778/mbio.02110-23.f004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/947b/10653832/0cf56fa7310a/mbio.02110-23.f005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/947b/10653832/829e9db468a5/mbio.02110-23.f006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/947b/10653832/579b87c50e4d/mbio.02110-23.f007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/947b/10653832/0e4edf5bc512/mbio.02110-23.f008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/947b/10653832/6913d81de619/mbio.02110-23.f009.jpg

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