Departamento de Infectómica y Patogénesis Molecular, CINVESTAV-IPN, México, D.F., Mexico.
Virology. 2013 Aug 1;442(2):132-47. doi: 10.1016/j.virol.2013.04.003. Epub 2013 May 2.
Several cellular molecules and components, specifically, cholesterol and lipid rafts have been described as necessary elements for dengue virus entry and signaling in several human cells. Thus, changes in lipid rafts formation and cholesterol levels were evaluated. Here we report that the amount of total cholesterol and lipid rafts formation increase early after infection of Huh-7 cells. This augment correlates with an increase in the amount of low density lipoprotein receptor (LDLr) on the surface of infected cells and also with a lower phosphorylation level of the 3-hydroxy-3-methyl-glutaryl-CoA reductase (HMGCR). None of the changes were observed in Huh 7 cells infected with VSV used as a control. These results suggest that dengue virus infection increases intracellular cholesterol levels at early times post infection by triggering the modulation of LDL particles uptake and the increase in the enzymatic activity of HMG-CoA reductase.
几种细胞分子和成分,特别是胆固醇和脂质筏,被描述为登革热病毒进入和在几种人类细胞中信号转导所必需的元素。因此,评估了脂质筏形成和胆固醇水平的变化。在这里,我们报告说,在 Huh-7 细胞感染后早期,总胆固醇的量和脂质筏的形成增加。这种增加与感染细胞表面低密度脂蛋白受体(LDLr)的量增加以及 3-羟基-3-甲基戊二酰辅酶 A 还原酶(HMGCR)的磷酸化水平降低相关。在用作为对照的 VSV 感染的 Huh 7 细胞中未观察到任何变化。这些结果表明,登革热病毒感染通过触发 LDL 颗粒摄取的调节和 HMG-CoA 还原酶的酶活性增加,在感染后早期增加细胞内胆固醇水平。