Department of Pathology, University of Virginia, Charlottesville, Virginia, United States of America.
Department of Biomedical Engineering, University of Virginia, Charlottesville, Virginia, United States of America.
PLoS One. 2020 Feb 7;15(2):e0228735. doi: 10.1371/journal.pone.0228735. eCollection 2020.
Influenza virus is an enveloped virus wrapped in a lipid bilayer derived from the host cell plasma membrane. Infection by influenza virus is dependent on these host cell lipids, which include sphingolipids. Here we examined the role of the sphingolipid, glucosylceramide, in influenza virus infection by knocking out the enzyme responsible for its synthesis, glucosylceramide synthase (UGCG). We observed diminished influenza virus infection in HEK 293 and A549 UGCG knockout cells and demonstrated that this is attributed to impaired viral entry. We also observed that entry mediated by the glycoproteins of other enveloped viruses that enter cells by endocytosis is also impaired in UGCG knockout cells, suggesting a broader role for UGCG in viral entry by endocytosis.
流感病毒是一种包裹在脂质双层中的包膜病毒，源自宿主细胞膜的质膜。流感病毒的感染依赖于这些宿主细胞脂质，包括神经酰胺。在这里，我们通过敲除负责其合成的酶，即葡萄糖神经酰胺合酶（UGCG），研究了神经酰胺在流感病毒感染中的作用。我们观察到，在 HEK 293 和 A549 UGCG 敲除细胞中，流感病毒感染减少，并证明这归因于病毒进入受损。我们还观察到，通过内吞作用进入细胞的其他包膜病毒的糖蛋白介导的进入也在 UGCG 敲除细胞中受损，这表明 UGCG 在通过内吞作用进入病毒方面发挥了更广泛的作用。
