CLN7/MFSD8可能是新冠病毒进入细胞的一个重要因素。
CLN7/MFSD8 may be an important factor for SARS-CoV-2 cell entry.
作者信息
Heinl Elena-Sofia, Lorenz Sebastian, Schmidt Barbara, Nasser M Laqtom Nouf, Mazzulli Joseph R, Francelle Laetitia, Yu Timothy W, Greenberg Benjamin, Storch Stephan, Tegtmeier Ines, Othmen Helga, Maurer Katja, Steinfurth Malin, Witzgall Ralph, Milenkovic Vladimir, Wetzel Christian H, Reichold Markus
机构信息
Medical Cell Biology, University Regensburg, 93053 Regensburg, Germany.
Institute of Clinical Microbiology and Hygiene, University of Regensburg, 93053 Regensburg, Germany.
出版信息
iScience. 2022 Oct 21;25(10):105082. doi: 10.1016/j.isci.2022.105082. Epub 2022 Sep 6.
The SARS-CoV-2 virus has triggered a worldwide pandemic. According to the BioGrid database, CLN7 (MFSD8) is thought to interact with several viral proteins. The aim of this work was to investigate a possible involvement of CLN7 in the infection process. Experiments on a CLN7-deficient HEK293T cell line exhibited a 90% reduced viral load compared to wild-type cells. This observation may be linked to the finding that CLN7 ko cells have a significantly reduced GM1 content in their cell membrane. GM1 is found highly enriched in lipid rafts, which are thought to play an important role in SARS-CoV-2 infection. In contrast, overexpression of CLN7 led to an increase in viral load. This study provides evidence that CLN7 is involved in SARS-CoV-2 infection. This makes it a potential pharmacological target for drug development against COVID-19. Furthermore, it provides insights into the physiological function of CLN7 where still only little is known about.
严重急性呼吸综合征冠状病毒2（SARS-CoV-2）引发了全球大流行。根据生物网格数据库，CLN7（MFSD8）被认为与多种病毒蛋白相互作用。这项工作的目的是研究CLN7在感染过程中可能发挥的作用。在CLN7缺陷的HEK293T细胞系上进行的实验表明，与野生型细胞相比，病毒载量降低了90%。这一观察结果可能与CLN7基因敲除细胞细胞膜中GM1含量显著降低的发现有关。GM1在脂筏中高度富集，而脂筏被认为在SARS-CoV-2感染中起重要作用。相反，CLN7的过表达导致病毒载量增加。这项研究提供了证据表明CLN7参与了SARS-CoV-2感染。这使其成为开发抗COVID-19药物的潜在药理学靶点。此外，它还为人们对仍知之甚少的CLN7的生理功能提供了见解。
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