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SARS-CoV-2 与人类靶细胞的相互作用——代谢视角。

Interactions of SARS-CoV-2 with Human Target Cells-A Metabolic View.

机构信息

Structural Membrane Biochemistry, Bavarian NMR Center (BNMRZ), Department of Bioscience, TUM School of Natural Sciences, Technical University of Munich, Lichtenbergstr. 4, 85747 Garching, Germany.

Chair of Microbiology, Biocenter, University of Würzburg, 97074 Würzburg, Germany.

出版信息

Int J Mol Sci. 2024 Sep 16;25(18):9977. doi: 10.3390/ijms25189977.

Abstract

Viruses are obligate intracellular parasites, and they exploit the cellular pathways and resources of their respective host cells to survive and successfully multiply. The strategies of viruses concerning how to take advantage of the metabolic capabilities of host cells for their own replication can vary considerably. The most common metabolic alterations triggered by viruses affect the central carbon metabolism of infected host cells, in particular glycolysis, the pentose phosphate pathway, and the tricarboxylic acid cycle. The upregulation of these processes is aimed to increase the supply of nucleotides, amino acids, and lipids since these metabolic products are crucial for efficient viral proliferation. In detail, however, this manipulation may affect multiple sites and regulatory mechanisms of host-cell metabolism, depending not only on the specific viruses but also on the type of infected host cells. In this review, we report metabolic situations and reprogramming in different human host cells, tissues, and organs that are favorable for acute and persistent SARS-CoV-2 infection. This knowledge may be fundamental for the development of host-directed therapies.

摘要

病毒是专性细胞内寄生虫,它们利用宿主细胞的细胞途径和资源来生存和成功繁殖。病毒利用宿主细胞代谢能力进行自身复制的策略可能有很大差异。病毒引发的最常见的代谢改变会影响受感染宿主细胞的中心碳代谢,特别是糖酵解、戊糖磷酸途径和三羧酸循环。上调这些过程的目的是增加核苷酸、氨基酸和脂质的供应,因为这些代谢产物对病毒的有效增殖至关重要。然而,这种操作可能会影响宿主细胞代谢的多个位点和调节机制,这不仅取决于特定的病毒,还取决于受感染的宿主细胞类型。在这篇综述中,我们报告了有利于急性和持续性 SARS-CoV-2 感染的不同人类宿主细胞、组织和器官中的代谢情况和重编程。这些知识可能是开发针对宿主的治疗方法的基础。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cfd9/11432161/f923874f49af/ijms-25-09977-g001a.jpg

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