THE ROLE OF CYTOKIN STORM AND OXIDATIVE STRESS IN THE SPREAD OF SARS-COV INFECTION
Journal Title: Nature & Science - Year 2022, Vol 4, Issue 2
Abstract
SARS CoV infection is one of the most common and economically damaging and life-threatening infections of the last 100 years. To combat it, first of all, it is necessary to study the mechanisms that stimulate its development. For this purpose, the role of genomic changes and oxidative stress in the spread of SARS-CoV virus is investigated. During the spread of this disease, lung damage has been found to occur under a "cytokine storm" caused by active forms of oxygen. SARS virus binds to target cells via angiotensin converting enzyme-2 (ACE2). In the early stages of the disease, SARS viruses cause accumulation and activation of NLRP3-inflammation, which plays a leading role in the formation of the inflammatory response to the virus. During the cytokine storm phase, interleukins, monocytic hematopoietic protein MCP-1, macrophage inflammatory protein MIP-1a, TGF, CCL2, CXCL10, CNXL9, TNF-a continue to increase. SARS-CoV-3b protein and nonstructural protein 10 (nsp10) of COVID virus in mitochondria It promotes the formation of OAF. 3CLpro protease is also known to cause apoptosis in human promonocytes by increasing OAF formation. Activation of the NF-κB transcription factor through oxidative stress can lead to severe lung damage. Naturally, in response to oxidative stress, the antioxidant system is activated, resulting in the depletion of the enzymatic and non-enzymatic branches of the system. After acquaintance with this mechanism, the reason for the spread of SARS COV infection in patients with hypertension treated with ACE-2 blockers is known. The therapeutic effect of antioxidants in this disease is also accepted as an undeniable fact.
Authors and Affiliations
Mahira Firudin Amirova, Gulnara Sabir Dashdamirova, Ellada Eldar Huseynova, Rena Rufat Rahimova, Nigar Xizri Mikayılova
Keywords
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- EP ID EP759319
- DOI 10.36719/2707-1146/17/5-10
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