Srilagna Sarkar, Amity University Kolkata
Even though the novel coronavirus disease originates in the lungs, it may extend to other tissues and cause organ damage including cardiac injury, multiorgan failure, and even acute kidney injury, associating it with an increased risk of death. Although the COVID-19 tissue injury is not primarily mediated by any viral infection, it may result in inflammatory host immune response, driving hypercytokinemia and other aggressive inflammation affecting lung parenchymal cell, also diminishing the oxygen rate uptake by the lungs, endothelial cells damage resulting in endothelium and thrombotic evens with intravascular coagulation.
The complement system signifies the primary responsibility of the host immune system of SARS-COV-2 infection, but several pieces of evidence show there is unstrained activation of complement induced in the lungs and other tissues play a major role in acute and chronic inflammation including thrombus formation, intravascular coagulation, ultimately leading to death due to organ failure.
As protection from tissue injury, besides the efforts on finding an effective antivirus therapy, emphasis on limited tissue injury in severe COVID-19 should be expanded. As, Gonzalez-Nicholas et al – has emphasized, tissue-protective cilastatin against hyper inflammation and its potential to limit virus entry in target cells. However, the fact that COVID-19 patients are frequently with antibiotics may generate early data by conventionally treated COVID-19 patients and will give trials randomizing patients to receive their imipenem – whether cilastatin or some substitute antibiotic. As proof of Cilastatin tissue protection will require testing the compound itself.
Also read: Is Diabetes as dangerous and wicked as COVID-19?
Source: https://academic.oup.com/ckj/advance-article/doi/10.1093/ckj/sfaa196/5917718
Nice 👍
Good…. keep it up…. 👌👌👌