CELL-CELL FUSION DUE TO INFLUENZA HEMAGGLUTININ

被包膜病毒感染动物细胞在以下情况下部分完成 病毒基因组在融合后被输送到细胞中 细胞膜和病毒膜。这种膜融合事件是由一种 蛋白质：在流感的情况下是血凝素(HA)。除了……之外 病毒-细胞膜融合，HA还将介导细胞融合， 只要分子以足够的浓度存在于至少一种 这两个细胞膜通过适当的有限蛋白质分解来激活， 在pH和lt；5.表达流感病毒的细胞之间的融合 病毒血凝素(HA蛋白)和人红细胞(RBC) 通过转移和去猝灭脂质标记物和 细胞质标记。融合度、脂质连续性和 细胞质的连续性，只有在延迟一段时间后才明显：37℃时约30秒 DEG和pH均为4.9。上述研究通过以下方式继续进行 单细胞-细胞融合反应的方式多种多样。检查核聚变在 单项事件的级别增加了到目前为止还没有意识到的信息： 1)融合要么全有，要么一无所有：要么一对在给定的pH值下融合，要么 在脉冲之后，或者不会；没有证据表明部分融合。2) 中性的再酸化，在熔合失败后，导致融合 具有相同的滞后时间和时间进程；滞后时间与历史无关 暴露在酸碱度下。3)个体融合滞后时间和时间进程为 在速度和曲线形状上都具有广泛的异质性。4)融合是 从一个小的可逆的小孔开始。这些事实提供了新的 质子浓度的小幅增加导致了 融合细胞的百分比，但不改变滞后时间意味着 质子扮演着变构调节器的角色。事实是， 在一个短的质子脉冲表明聚变之后，反应继续进行，在 反应级联中的某个点是不可逆的。事实上，毛孔 在毛孔扩张过程中形成是可逆的和可变的，使病毒 蛋白质诱导的膜融合类似于 胞吐。

Infection of animal cells by enveloped viri is accomplished in part when the viral genome is delivered into the cell following the fusion of the cell and viral membranes. This membrane fusion event is catalysed by a protein: in the case of influenza the hemagluttinin (HA). In addition to viral-cell membrane fusion, HA will also mediate the fusion of cells, provided the molecule exists in sufficient concentration in at least one of the two cell membranes, is activated by appropriate limited proteolysis, and is protonated at pH < 5. Fusion between cells expressing influenza virus hemagluttinin (HA protein), and human red blood cell (RBC) was detected by the transfer and dequenching of both a lipid marker and a cytoplasmic marker. Both measures of fusion, lipid continuity and cytoplasmic continuity, were evident only after a delay: about 30 sec at 37 deg and pH 4.9. The studies outlined above have been continued by following single cell-cell fusion reactions in various ways. Examining fusion at the level of single events adds information which was not appreciated hitherto: 1) Fusion is all or nothing: either a pair will fuse at a given pH, or after a pulse, or it will not; there is no evidence of partial fusion. 2) Reacidification from neutrality, following failure to fuse, leads to fusion with the same lag time and time-course; Lag time is independent of history of exposure to pH. 3) Individual fusion lag times and time-courses are broadly heterogeneous, both in rate and shape of curve. 4) Fusion is initiated with a small, reversible pore. These facts provide new constraints on the possible mechanisms of fusion. Primarily, the fact that a small increase in proton concentration caused a large increase in the percentage of fusing cells, but does not change the lag time implies that protons are playing the role of an allosteric modulator. The fact that the reaction continues after a short pulse of protons indicates the fusion, at some point in the reaction cascade, is irreversible. The fact that pore formation is reversible and variable during pore widening makes the viral protein induced membrane fusion similar to the membrane fusion pore seen in exocytosis.