AI Article Synopsis
- Severe COVID-19 is associated with a heightened immune response, especially in patients with conditions like obesity and diabetes, resulting in poor health outcomes.
- Chronic inflammation due to cardiometabolic issues leads to increased levels of pro-inflammatory cytokines like IL-6 and TNF-α, primarily through the Toll-Like Receptors 4 (TLR4) pathway.
- The spike protein of SARS-CoV-2 interacts with TLR4, triggering a severe immune reaction that can cause respiratory distress, cytokine storms, and potential damage to multiple organs.
Article Abstract
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.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7505161 | PMC |
| http://dx.doi.org/10.1016/j.cytogfr.2020.09.002 | DOI Listing |
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