• November 6, 2021

Sars cov 2 mip1a

Severe acute respiratory syndrome coronavirus 2 (SARS-Cov-2) is the pathogen that causes coronavirus disease 2019 (COVID-19). As of May 25, 2020, the COVID-19 outbreak has caused 347,192 deaths worldwide. Current evidence showed that severely ill patients tend to have a high concentration of pro-inflammatory cytokines, such as interleukin (IL) -6, compared to those who are moderately ill.

The high level of cytokines also indicates a poor prognosis in COVID-19. Furthermore, excessive infiltration of pro-inflammatory cells, mainly macrophages and T-helper cells 17, has been found in lung tissues of COVID-19 patients by post-mortem examination. Recently, more and more studies indicate that the “cytokine storm” may contribute to COVID-19 mortality. Here, we summarize the clinical and pathological features of the cytokine storm in COVID-19.

Our review shows that SARS-Cov-2 selectively induces a high level of IL-6 and results in lymphocyte depletion. Current evidence indicates that tocilizumab, an IL-6 inhibitor, is relatively effective and safe. In addition, corticosteroids, programmed cell death protein (PD) -1 / PD-L1 checkpoint inhibition, cytokine adsorption devices, intravenous immunoglobulin, and antimalarial agents could be potentially useful and reliable approaches to counteract the cytokine storm in COVID-19 patients.

Introduction

In December 2019, an outbreak of a new coronavirus-based disease was reported in Wuhan, China. On February 11, 2020, the World Health Organization (WHO) named this coronavirus “severe acute respiratory syndrome coronavirus 2” (SARS-CoV-2) and the disease that caused “coronavirus disease 2019” (COVID-19 ). As of May 25, 2020, SARS-CoV-2 has affected more than 212 countries and around 5,529,195 cases have been confirmed worldwide, of which 347,192 people have died.

The reason for these deaths is suspected to be “cytokine storm” [also called “cytokine storm syndrome” (CSS)]. The International Classification of Diseases (ICD) does not include the Cytokine Storm or CSS. Cron and Behrens bring current knowledge of CSS (1). They define that the “cytokine storm” as a cascade of activation of the production of self-amplified cytokines due to the host’s unregulated immune response to different triggers.

Triggers involved infections, malignancy, rheumatic disorders, etc. Another scholar described that cytokine storm is a systemic inflammatory response to infections and drugs and leads to excessive activation of immune cells and the generation of pro-inflammatory cytokines (2). A similar entity is called “cytokine release syndrome” (CRS), which is not defined in the CSS textbook (1).

CRS is an acute systemic inflammatory syndrome characterized by multiple organ dysfunction (MOD). Chimeric antigen receptor (CAR) T-cell therapy has been reported to help distinguish CRS from a cytokine storm (2). Of note, the textbook described the criteria for CSS based on hemophagocytic lymphohistiocytosis (HLH) and secondary HLH (Shih) associated with rheumatic disorders, such as macrophage activation syndrome (MAS) (1).

Therefore, it may not be applicable in COVID-19 because of COVID-19 contagious disease and relatively irrelevant to a genetic disorder. To date, clinical and laboratory criteria to identify the cytokine storm are still lacking. In this review, we refer to the COVID-19 associated cytokine storm as severely ill patients along with a high concentration of pro-inflammatory cytokines.

For COVID-19 patients, the number of white blood cells, neutrophils, as well as levels of procalcitonin, C-reactive protein, and other inflammatory indices, are significantly higher in the intensive care unit (ICU) cases than in ICUs. who are not in the ICU? cases (3, 4). Many studies showed that severely ill patients tended to have a higher concentration of pro-inflammatory cytokines, especially interleukin (IL) 6, than moderately ill COVID-19 patients (5-9).

The bronchoalveolar lavage fluid (BALF) cell result, which was analyzed by transcriptome sequencing, reveals excessive chemokine release caused by SARS-CoV-2 infection, such as CXCL10 and CCL2 (10). The high level of cytokines also indicates a poor prognosis in COVID-19 (6, 11, 12). In addition, the pathology of the post-mortem examination of the lung, of the person who died from COVID-19, demonstrated the existence of respiratory distress syndrome.

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