The severe form of COVID-19 is marked by an abnormal and exacerbated immunological host response favoring to a poor outcome in a significant number of patients, especially those with obesity, diabetes, hypertension, and atherosclerosis. The chronic inflammatory process found in these cardiometabolic comorbidities is marked by the overexpression of pro-inflammatory cytokines such as interleukin-6 (IL-6) and tumoral necrosis factor-alpha (TNF-α), which are products of the Toll-Like receptors 4 (TLR4) pathway. The SARS-CoV-2 initially infects cells in the upper respiratory tract and, in some patients, spread very quickly, needing respiratory support and systemically, causing collateral damage in tissues. We hypothesize that this happens because the SARS-CoV-2 spike protein interacts strongly with TLR4, causing an intensely exacerbated immune response in the host's lungs, culminating with the cytokine storm, accumulating secretions and hindering blood oxygenation, along with the immune system attacks the body, leading to multiple organ failure.

重症 COVID-19 的特点是异常和加剧的免疫宿主反应，导致大量患者预后不良，尤其是那些患有肥胖症、糖尿病、高血压和动脉粥样硬化的患者。在这些心脏代谢合并症中发现的慢性炎症过程的特征是促炎细胞因子的过度表达，例如白细胞介素 6 (IL-6) 和肿瘤坏死因子-α (TNF-α)，它们是 Toll 样受体的产物4 (TLR4) 通路。SARS-CoV-2 最初感染上呼吸道的细胞，在一些患者中传播速度非常快，需要呼吸支持和全身性的支持，从而对组织造成附带损害。我们假设发生这种情况是因为 SARS-CoV-2 刺突蛋白与 TLR4 强烈相互作用，