Recent studies have shown that SARS-CoV-2 virus can be inactivated by effect of heat, even though, little is known about the molecular changes induced by the temperature. Here, we unravel the basics of such inactivation mechanism over the SARS-CoV-2 spike glycoprotein by executing atomistic molecular dynamics simulations. Both the closed down and open up states, which determine the accessibility to the receptor binding domain, were considered. Results suggest that the spike undergoes drastic changes in the topology of the hydrogen bond network while salt bridges are mainly preserved. Reorganization in the hydrogen bonds structure produces conformational variations in the receptor binding subunit and explain the thermal inactivation of the virus. Conversely, the macrostructure of the spike is preserved at high temperature because of the retained salt bridges. The proposed mechanism has important implications for engineering new approaches to inactivate the SARS-CoV-2 virus.

中文翻译：

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温度导致SARS-CoV-2失活的分子机理

最近的研究表明，即使对温度引起的分子变化知之甚少，SARS-CoV-2病毒也可以通过热作用灭活。在这里，我们通过执行原子分子动力学模拟，揭示SARS-CoV-2穗状糖蛋白失活机制的基础。同时考虑了关闭状态和打开状态，它们决定了受体结合结构域的可及性。结果表明，尖峰在氢键网络的拓扑结构中发生了剧烈变化，而盐桥主要保留下来。氢键结构的重组在受体结合亚基中产生构象变化，并解释了病毒的热失活。反过来，由于保留了盐桥，因此尖峰的宏观结构在高温下得以保留。拟议的机制对工程设计灭活SARS-CoV-2病毒的新方法具有重要意义。