Fusion of viral membrane with host cell membrane

With the transition of gp41 into the six-helix bundle, fusion of the viral and target cell membranes begins to take place. The specifics of fusion are not completely clear, but it is understood that fusion proceeds after insertion of the gp41 fusion peptide, which results in curvature of viral and target cell membranes. This results in a state of hemi-fusion, where only the outer lipid bilayers of each membrane are fused, whereas membrane leaflets that are distal with respect to the intermembrane gap remain separate at this stage. Hemi-fusion allows the exchange of lipids between the contacting leaflets, whereas the exchange of aqueous content between the virus and the cell remains blocked. The next step in fusion is the merger of the distal leaflets, leading to the formation of a nascent fusion pore, which leads to mixing of viral and cellular contents. Studies of fusion of Influenza virus suggested that multiple hairpin structures may form a narrow fusion pore which subsequently expands to a larger opening. In the case of HIV, this larger opening allows for passage of the Matrix-surrounded viral core out of the virus and into the host cell cytoplasm.

随着gp41跨膜蛋白转变为六螺旋束结构，病毒与靶细胞膜融合的进程开始启动。融合的具体机制尚不明确，然而，融合过程是在gp41融合肽插入之后发生的，导致病毒和靶细胞膜发生弯曲。这一过程导致半融合状态的形成，此时，仅每个膜的脂质双层外层发生融合，而相对于膜间隙的远端膜叶在此阶段保持分离。半融合状态允许接触叶之间的脂质交换，而病毒与细胞之间的水溶性物质交换则受到阻碍。融合的下一步是远端叶的融合，进而形成初生的融合孔，导致病毒和细胞内容物的混合。对流感病毒融合的研究表明，多个发夹结构可能形成狭窄的融合孔，随后该孔径扩大至更大。在HIV的情况下，这个更大的开口允许被基质蛋白包围的病毒核心从病毒颗粒中逸出，进入宿主细胞的细胞质中。