Wang W, Fu Y J, Zu Y G, Wu N, Reichling J, Efferth T
Northeast Forestry University, Harbin, People's Republic of China.
Arch Virol. 2009;154(4):595-600. doi: 10.1007/s00705-009-0348-2. Epub 2009 Mar 15.
Lipid rafts are involved in the life cycle of many viruses. In this study, we investigated the role of lipids in the life cycle of vesicular stomatitis virus (VSV). Cholesterol depletion by pretreatment of BHK cells or VSV particles with methyl-beta-cyclodextrin (MbetaCD), a cholesterol-sequestering drug, inhibited the production of VSV dramatically. This effect was reversible, and virus production was restored by the addition of cholesterol, indicating that the reduction was caused by the loss of cholesterol in the cell membrane and virus, respectively. Cholesterol depletion at the adsorption stage also reduced the production of VSV significantly, but in contrast, only had a limited effect on virus production at the post-entry stage. Inhibition of sphingomyelin by myriocin treatment only showed a minor effect on VSV production. However, reduction of cholesterol and sphingomyelin at the same time dramatically reduced VSV production, showed a significant synergistic effect. These results suggest that lipid rafts play an important role in the life cycle of VSV.
脂筏参与许多病毒的生命周期。在本研究中，我们调查了脂质在水疱性口炎病毒（VSV）生命周期中的作用。用胆固醇螯合剂甲基-β-环糊精（MβCD）预处理BHK细胞或VSV颗粒来消耗胆固醇，可显著抑制VSV的产生。这种效应是可逆的，添加胆固醇后病毒产生得以恢复，表明产量降低分别是由细胞膜和病毒中胆固醇的丢失所致。在吸附阶段消耗胆固醇也显著降低了VSV的产量，但相比之下，对进入后阶段的病毒产量仅有有限的影响。用肉豆蔻素处理抑制鞘磷脂仅对VSV产量显示出轻微影响。然而，同时降低胆固醇和鞘磷脂会显著降低VSV产量，显示出显著的协同效应。这些结果表明脂筏在VSV的生命周期中起重要作用。
