In the present work we propose a dynamical mathematical model of the lung cells inflammation process in response to SARS-CoV-2 infection. In this scenario, our model suggests that the main protease Nsp5 enhances the inflammatory process by increasing the levels of NF κB, IL-6, Cox2, and PGE2 with respect to a reference state without the virus. This overstimulated immune state becomes autonomous of the signals from other immune cells, and does not shut down by itself neither when the external signals are turned off. Our model suggests that Nsp5 is effectively the switch to start inflammation, the consequent overproduction of the ACE2 receptor, and an important underlying cause of the most severe cases of COVID19.
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