Ayodeji-Durojaye, Olanrewaju

Language: Spanish
References: 7
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Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) has demonstrated a similar infection pattern (with a faster rate of transmission) and clinical features compared to Severe Acute Respiratory Syndrome Coronavirus (SARS-CoV) and Middle East Respiratory Syndrome Coronavirus (MERS-CoV). However, it is of utmost interest that acute respiratory distress syndrome (ARDS), systemic inflammatory response syndrome (SIRS) and acute lung injury (ALI) occurred in both MERS-CoV- and SARS-CoV-infected individuals, as well as Coronavirus Disease-19 (COVID-19) patients.(1) Specific cytokines have been observed at the core of inflammation development and have also been found to play critical roles in facilitating the exhibition of the aforementioned clinical features. According to reports from previous studies, cytokines such as Tumor Necrosis Factor-α (TNF-α), Macrophage Inflammatory Protein-1A (MIP-1A), monocyte chemoattractant protein-1 (MCP-1), IFN-γ-Inducible Protein 10 (IP10), Granulocyte colony-stimulating factor (GSCF), Interleukin-2 (IL-2), Interleukin-7 (IL-7), Interleukin-10 (IL-10) and Interleukin-17 (IL-17) are significantly increased in COVID-19 patients, with the attributes of a cytokine storm. Upon infection by SARS-CoV-2, the inflammatory response plays an antiviral function, but an intense cytokine storm as a result of imbalanced response, could have a harmful effect on patients. Therefore, employing approaches that suppresse effectively cytokine storm is required for saving the COVID-19 patients’ lives and to prevent disease deterioration, which is of great significance to reduce mortality rate and for treating patients with severe infection. Elucidation of the mechanism of the SARS-CoV-2-induced cytokine storm may shed more light on the potential therapeutic interventions towards the quelling and prevention of this hazardous process.

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