Ruigrok R W, Hirst E M, Hay A J
National Institute for Medical Research, Mill Hill, London, U.K.
J Gen Virol. 1991 Jan;72 ( Pt 1):191-4. doi: 10.1099/0022-1317-72-1-191.
Amantadine specifically inhibits the release of virus particles from cells infected with the Rostock (H7N1) strain of influenza A virus, apparently as a consequence of a membrane protein M2-mediated conversion of haemagglutinin (HA) to its low pH conformation. Electron microscopic observations, together with immunogold labelling, showed that amantadine action does not alter the distribution of HA on the cell surface nor does it prevent the formation of budding virus particles. It was not possible, however, to discern whether low pH HA inhibited the final stage in virus maturation, i.e. pinching off, or simply prevented release of fully formed particles.
金刚烷胺特异性抑制甲型流感病毒罗斯托克(H7N1)株感染的细胞中病毒颗粒的释放,这显然是由于膜蛋白M2介导的血凝素(HA)向其低pH构象转化的结果。电子显微镜观察以及免疫金标记显示,金刚烷胺的作用不会改变HA在细胞表面的分布,也不会阻止出芽病毒颗粒的形成。然而,无法确定低pH的HA是抑制了病毒成熟的最后阶段,即掐断过程,还是仅仅阻止了完全形成的颗粒的释放。