Most severe cases with COVID-19, especially those with pulmonary failure, are not a consequence of viral burden and/or failure of the ‘adaptive’ immune response to subdue the pathogen by utilizing an adequate ‘adaptive’ immune defense. Rather it is a consequence of immunopathology, resulting from imbalanced innate immune response, which may not be linked to pathogen burden at all. In fact, it might be described as an autoinflammatory disease. The Kawasaki-like disease seen in children with SARS-CoV-2 exposure might be another example of similar mechanism.

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关于 COVID-19 的遗传学和免疫发病机制。

大多数 COVID-19 重症病例，尤其是肺功能衰竭病例，并不是病毒负荷和/或“适应性”免疫反应未能利用充分的“适应性”免疫防御来抑制病原体的结果。相反，它是免疫病理学的结果，由先天免疫反应失衡引起，可能与病原体负担根本无关。事实上，它可能被描述为一种自身炎症性疾病。在接触过 SARS-CoV-2 的儿童中观察到的川崎样病可能是类似机制的另一个例子。