Polymorphisms in the inter leukin-1 beta gene (rs16944 and rs1143627) as a risk factor for SARS-COV2 infection

Despite evidence of cytokine gene variation in SARS-CoV-2 sickness is few, understanding the function of genetic polymorphisms in the course of respiratory infections may aid in the identification of possible andidates for future inquiry in SARS-CoV-2 patients. As a result, the study raises crucial issues about how cytokine gene polymorphisms may have a role in the severity of COVID-19 sickness. ARMS-PCR was used to detect genotype frequency data for the IL-1B SNP (rs 16944), (rs1143627). All data statistical analyses were performed using the Statistical Package for Social Science (SPSS 26).. shows the genotype distributions (frequencies) of the chosen IL-1B SNPs, rs16944 A/G and rs1143627 G/A, as well as their relationships with SARS-COV2 risk. Significant relationships between the rs16944 A/G and SARS-COV2 risk were found in the samples, The AG variant genotype (AG vs. AA) showed an adjusted OR of 1.0 (95 percent CI = 1.770 (0.935-0.353), P = 0.078*) when compared to the rs16944 AA genotype. There were no statistical differences in rs1143627 polymorphism between the two groups, and there was no evidence that rs1143627 may be associated with an increased risk of acquiring SARS-COV2 based on the results of the p value G (P = 0.167), G/A (P = 0.22), and G/G (P = 0.22). This was the first study to look at the rs1143627 polymorphism in relation to SARS-COV 2, therefore no previous research was published.first, second, and third level headings (first level heading). © 2023 Author(s).

Significance of Measuring the Proinflammatory Response Biomarkers in Covid-19 Patients

Objectives: In the management of COVID-19, bio-inflammatory cytokines (IL-6 and others) can be measured as inflammatory markers to detect conditions in response to treatment, risk assessment, monitoring disease progression, prognosis determination and treatment selection. The purpose of this study is to identify changes in inflammation markers of COVID-19 patients and to determine whether it should be used as a prognosis marker. Materials-Methods: Three groups of the patients consisting of 138 patients (12 non-survived, 35 severe and 91 mild/moderate) aged 16 to 86 years who were diagnosed with COVID-19 by real-time polymerase chain reaction were included in the study. Acute phase serum levels such as CRP, D-Dimer, Ferritin, IL-1B and IL-6 were measured and compared in serum samples taken from these patients. It was examined whether these parameters can be a biomarker that can be monitored for the course of the disease. IL-6 and ferritin were measured with CLIA, D-dimer immunassay, CRP with photometry and IL1-B was measured with flow cytometry methods. Result(s): It has been observed that all parameters, except for ferritin (P=0.94), increase significantly during the transition from mild to severe form of the disease. (CRP P:0.005, D-Dimer P<0.0001, IL-1B P:0.03, IL-6 P:0.002). A significant difference was observed in the levels of CRP, IL-6 and D-Dimer in the patient survival. (P=0.003, P=0.03, P:0,0001). According to our results, the use of IL-1B in the prognosis monitoring of patients with severe forms was not found to be significant (P:0.48). ROC curve analysis showed that the area under the ROC curve (AUC) of CRP, D-Dimer and IL-6 was 0.645 (0,559 to 0,725), 0.637 (0,551 to 0,717) and 0.663 (0,577 to 0,741) respectively, and the cutoff values were >3.77 (sensitivity, 72.3%;specificity, 55%), >0.48 (sensitivity 68.1%;specificity, 57.1%) and <14.9 (sensitivity, 65,9%;specificity, 62.6%), respectively. Conclusion(s): Our results confirmed that the dynamic change in IL-6, CRP, D-Dimer can be used as a marker for disease monitoring in patients with severe COVID-19.

Inflammasomes and IL-1 family cytokines in SARS-CoV-2 infection: from prognostic marker to therapeutic agent.

Despite global vaccination programs, infections with severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) continue to cause severe disease with significant morbidity and mortality. Severe coronavirus disease 2019 (COVID-19) is characterized by an exuberant inflammatory response in the lung leading to acute lung injury and consequent gas exchange problems. Complete insights in this hyperinflammatory response are still lacking. However, a thorough understanding of immunopathogenesis of severe COVID-19 is needed to not only develop personalized targeted therapies, but also to identify biomarkers that predict disease outcome and therapeutic responses. Here we review the current evidence that SARS-CoV-2 activates the inflammasome, which is an intracellular multiprotein complex that leads to the activation and secretion of the interleukin (IL)-1 family cytokines, IL-1ß and IL-18, and to a lytic form of cell death, called pyroptosis. Further we discuss the contribution of inflammasomes and IL-1 family cytokines to the immunopathogenesis of COVID-19 and its clinical implications.

MicroRNAs based regulation of cytokine regulating immune expressed genes and their transcription factors in COVID-19.

BACKGROUND: Coronavirus disease 2019 is characterized by the elevation of a broad spectrum of inflammatory mediators associated with poor disease outcomes. We aimed at an in-silico analysis of regulatory microRNA and their transcription factors (TF) for these inflammatory genes that may help to devise potential therapeutic strategies in the future. METHODS: The cytokine regulating immune-expressed genes (CRIEG) were sorted from literature and the GEO microarray dataset. Their co-differentially expressed miRNA and transcription factors were predicted from publicly available databases. Enrichment analysis was done through mienturnet, MiEAA, Gene Ontology, and pathways predicted by KEGG and Reactome pathways. Finally, the functional and regulatory features were analyzed and visualized through Cytoscape. RESULTS: Sixteen CRIEG were observed to have a significant protein-protein interaction network. The ontological analysis revealed significantly enriched pathways for biological processes, molecular functions, and cellular components. The search performed in the miRNA database yielded ten miRNAs that are significantly involved in regulating these genes and their transcription factors. CONCLUSION: An in-silico representation of a network involving miRNAs, CRIEGs, and TF, which take part in the inflammatory response in COVID-19, has been elucidated. Thus, these regulatory factors may have potentially critical roles in the inflammatory response in COVID-19 and may be explored further to develop targeted therapeutic strategies and mechanistic validation.

Do inflammasome impact COVID-19 severity?

COVID-19 pandemic has proven to be a dramatic challenge, introducing huge clinical differences that demand extensive investigations. Severe and critical patients may present coagulopathies and microthrombi, which results in varied complications, or acute respiratory distress syndrome that leads to fatality. Although the lung to be the major site of clinical manifestations, COVID-19 has shown extrapulmonary manifestations, especially on the heart and kidney, directly linked to worse disease outcomes. According to the fast-moving of clinical description and scientific publications, the injuries in multiple organs and systemic inflammation appear to be caused by a deregulated immune response, and the NLRP3 inflammasome could be a relevant influencer in this imbalance. However, until now, the precise drivers of the pathophysiology of these injuries remain unknown. In this review, we discuss how inflammasome seems to be directly involved in the clinical profile of patients infected with SARS-CoV-2 and shed light on the mechanisms that lead to fatality.