Department of Microbiology, Faculty of Medicine Siriraj Hospital, Mahidol University, 2 Prannok Road, Bangkok, 10700, Thailand.
Faculty of Medicine and Public Health, HRH Princess Chulabhorn College of Medical Science, Chulabhorn Royal Academy, Bangkok, Thailand.
Arch Virol. 2020 May;165(5):1151-1161. doi: 10.1007/s00705-020-04596-5. Epub 2020 Mar 29.
Influenza A virus (IAV) depends on the metabolism of its cellular host to provide energy and essential factors, including lipids, for viral replication. Previous studies have shown that fatty acids (FAs) play an important role in IAV replication and that inhibition of FA biosynthesis can diminish viral replication. However, cellular lipids can either be synthesized intracellularly or be imported from the extracellular environment. Interfering with FA import mechanisms may reduce the cellular lipid content and inhibit IAV replication. To test this hypothesis, MDCK and Detroit 562 cells were infected with IAV followed by exposure to palmitic acid and inhibitors of FA import. Replication of IAV significantly increased when infected cells were supplied with palmitic acid. This enhancement could be reduced by adding an FA import inhibitor. The addition of palmitic acid significantly increased the cellular lipid content, and this increased level was reduced by treatment with an FA import inhibitor. These results show that reducing the cellular lipid level might be an approach for IAV therapy.
甲型流感病毒(IAV)依赖于宿主细胞的代谢来提供能量和必要的因子,包括脂质,以进行病毒复制。先前的研究表明,脂肪酸(FAs)在 IAV 复制中起着重要作用,抑制 FA 生物合成可以减少病毒复制。然而,细胞内的脂质可以在细胞内合成,也可以从细胞外环境中输入。干扰 FA 输入机制可能会降低细胞内脂质含量并抑制 IAV 复制。为了验证这一假说,用 IAV 感染 MDCK 和 Detroit 562 细胞,然后用棕榈酸和 FA 输入抑制剂处理。当感染细胞提供棕榈酸时,IAV 的复制明显增加。添加 FA 输入抑制剂可以减少这种增强作用。添加棕榈酸可显著增加细胞内脂质含量,而用 FA 输入抑制剂处理可降低这种增加水平。这些结果表明,降低细胞内脂质水平可能是 IAV 治疗的一种方法。