Sato T, Serizawa T, Okahata Y
Department of Biomolecular Engineering, Tokyo Institute of Technology, Yokohama, Japan.
Biochim Biophys Acta. 1996 Nov 13;1285(1):14-20. doi: 10.1016/s0005-2736(96)00138-1.
The binding of influenza A virus to GM3-containing monolayers at an air/water interface was quantitatively investigated by use of a quartz crystal microbalance (QCM). A QCM was horizontally attached to the monolayer from the air phase and the binding behavior of influenza virus was followed by the frequency changes of the QCM. GM3 was reconstituted in the momolayer of sphingomyelin (SM) or glucosylceramide (GlcCer). When the mole fraction of GM3 was below 30 mol%, the binding rate of the influenza A virus to the GM3/GlcCer membrane was significantly faster than that to GM3/SM membranes. When the mole fraction of GM3 in SM was below 20 mol%, specific binding of influenza virus was not observed at all. Binding of the virus to the GM3/GlcCer mixed membrane was inhibited by the addition of sialyllactose (Neu5Ac alpha 2-3Gal beta 1-4Glc). The virus binding was also visually observed by scanning electron microscopy. Viruses selectively bound to GM3/GlcCer (20:80, by mol%) membrane, but not to GM3/SM (20:80, by mol%) membrane. Furthermore, it was suggested that specific binding of influenza virus to the GM3/GlcCer membrane induced the changes in morphology of virus. It was clearly demonstrated that binding of influenza virus to GM3 was influenced by matrix lipids surrounding GM3.
利用石英晶体微天平（QCM）对甲型流感病毒在气/水界面与含GM3的单层膜的结合进行了定量研究。将QCM从气相水平附着到单层膜上，通过QCM的频率变化跟踪流感病毒的结合行为。GM3在鞘磷脂（SM）或葡萄糖神经酰胺（GlcCer）的单层膜中重构。当GM3的摩尔分数低于30 mol%时，甲型流感病毒与GM3/GlcCer膜的结合速率明显快于与GM3/SM膜的结合速率。当SM中GM3的摩尔分数低于20 mol%时，根本未观察到流感病毒的特异性结合。通过添加唾液乳糖（Neu5Acα2-3Galβ1-4Glc）可抑制病毒与GM3/GlcCer混合膜的结合。还通过扫描电子显微镜直观观察到病毒结合情况。病毒选择性地结合到GM3/GlcCer（摩尔比为20:80）膜上，但不结合到GM3/SM（摩尔比为20:80）膜上。此外，提示流感病毒与GM3/GlcCer膜的特异性结合诱导了病毒形态的变化。清楚地表明，流感病毒与GM3的结合受GM3周围基质脂质的影响。
