Tosteson M T, Chow M
Department of Cell Biology, Harvard Medical School, Boston, Massachusetts 02115, USA.
J Virol. 1997 Jan;71(1):507-11. doi: 10.1128/JVI.71.1.507-511.1997.
The steps in poliovirus infection leading to viral entry and uncoating are not well understood. Current evidence suggests that the virus first binds to a plasma membrane-bound receptor present in viable cells, leading to a conformational rearrangement of the viral proteins such that the virus crosses the membrane and releases the genomic RNA. The studies described in this report were undertaken to determine if poliovirus (160S) as well as one of the subviral particles (135S) could interact with membranes lacking poliovirus receptors in an effort to begin to understand the process of uncoating of the virus. We report that both forms of viral particles, 160S and 135S, interact with lipid membranes and induce the formation of ion-permeable channels in a manner that does not require acid pH. The channels induced by the viral particles 160S have a voltage-dependent conductance which depends on the ionic composition of the medium. Our findings raise the possibility that viral entry into cells may be mediated by direct interaction of viral surface proteins with membrane lipids.
导致脊髓灰质炎病毒进入细胞并脱壳的感染步骤尚未完全明确。目前的证据表明，该病毒首先与活细胞中存在的质膜结合受体结合，导致病毒蛋白发生构象重排，从而使病毒穿过细胞膜并释放基因组RNA。本报告中描述的研究旨在确定脊髓灰质炎病毒（160S）以及一种亚病毒颗粒（135S）是否能与缺乏脊髓灰质炎病毒受体的膜相互作用，以便开始了解病毒脱壳的过程。我们报告，两种形式的病毒颗粒，即160S和135S，都能与脂质膜相互作用，并以不依赖酸性pH的方式诱导形成离子通透通道。由病毒颗粒160S诱导的通道具有电压依赖性电导，这取决于介质的离子组成。我们的发现增加了一种可能性，即病毒进入细胞可能是由病毒表面蛋白与膜脂质的直接相互作用介导的。
