受体/辅助受体介导的包膜病毒进入机制
Mechanisms of receptor/coreceptor-mediated entry of enveloped viruses
摘要：
包膜病毒通过内吞作用或通过病毒膜包膜与宿主细胞膜的直接融合进入宿主细胞。然而，一些病毒，如HIV-1，HSV-1，和EB病毒可以进入细胞通过任一机制，与路径的选择往往是周围的物理化学条件的函数，如温度和pH值。我们开发了一个随机模型，描述了进入过程中的结合水平的病毒糖蛋白尖峰细胞膜受体和辅助受体。在我们的模型中，受体将细胞膜附着到病毒膜上，而随后的辅助受体的结合使融合成为可能。该模型量化了融合和内吞进入途径之间的竞争。在高病毒加标密度限度下，通过数值和分析计算各途径的相对概率。我们描绘参数制度，融合或内吞作用占主导地位。这些参数与可测量和潜在可控的量有关，如膜弯曲刚度和受体、辅助受体和病毒峰密度。我们的机械假说的实验影响提出和讨论。
英文摘要：
Enveloped viruses enter host cells either through endocytosis, or by direct fusion of the viral membrane envelope and the membrane of the host cell. However, some viruses, such as HIV-1, HSV-1, and Epstein-Barr can enter a cell through either mechanism, with the choice of pathway often a function of the ambient physical chemical conditions, such as temperature and pH. We develop a stochastic model that describes the entry process at the level of binding of viral glycoprotein spikes to cell membrane receptors and coreceptors. In our model, receptors attach the cell membrane to the viral membrane, while subsequent binding of coreceptors enables fusion. The model quantifies the competition between fusion and endocytotic entry pathways. Relative probabilities for each pathway are computed numerically, as well as analytically in the high viral spike density limit. We delineate parameter regimes in which fusion or endocytosis is dominant. These parameters are related to measurable and potentially controllable quantities such as membrane bending rigidity and receptor, coreceptor, and viral spike densities. Experimental implications of our mechanistic hypotheses are proposed and discussed.
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