tetano
Editor, Senior Moderator
Curr Pharm Des
. 2022 May 19.
doi: 10.2174/1381612828666220519150821. Online ahead of print.
Immunopathogenesis and immunogenetic variants in COVID-19
Pakorn Sagulkoo[SUP] 1 2 [/SUP], Kitiporn Plaimas[SUP] 3 4 [/SUP], Apichat Suratanee[SUP] 5 6 [/SUP], Andrea Name Colado Simão[SUP] 7 [/SUP], Edna Maria Vissoci Reiche[SUP] 7 [/SUP], Michael Maes[SUP] 8 9 10 [/SUP]
Affiliations
Abstract
Coronavirus disease 2019 (COVID-19) continues to spread globally despite the discovery of vaccines. Many people die due to COVID-19 as a result of catastrophic consequences, such as acute respiratory distress syndrome, pulmonary embolism, and disseminated intravascular coagulation caused by a cytokine storm. Immunopathology and immunogenetic research may assist in diagnosing, predicting, and treating severe COVID-19 and the cytokine storm associated with COVID-19. This paper reviews the immunopathogenesis and immunogenetic variants that play a role in COVID-19. Although various immune-related genetic variants have been investigated in relation to severe COVID-19, the NOD-like receptor protein 3 (NLRP3) and interleukin 18 (IL-18) have not been assessed for their potential significance in the clinical outcome. Here, we a) summarize the current understanding of the immunogenetic etiology and pathophysiology of COVID-19 and the associated cytokine storm; and b) construct and analyze protein-protein interaction (PPI) networks (using enrichment and annotation analysis) based on the NLRP3 and IL18 variants and all genes, which were established in severe COVID-19. Our PPI network and enrichment analyses predict a) useful drug targets to prevent the onset of severe COVID-19 including key antiviral pathways such as Toll-Like-Receptor cascades, NOD-like receptor signaling, RIG-induction of interferon (IFN) α/β, and interleukin (IL)-1, IL-6, IL-12, IL-18, and tumor necrosis factor signaling; and b) SARS-CoV-2 innate immune evasion and the participation of MYD88 and MAVS in the pathophysiology of severe COVID-19. The PPI network genetic variants may be used to predict more severe COVID-19 outcomes, thereby opening the door for targeted preventive treatments.
Keywords: COVID-19; IL-18.; NLRP3; SARS-CoV-2; cytokines storm; inflammation; variant genotypes.
. 2022 May 19.
doi: 10.2174/1381612828666220519150821. Online ahead of print.
Immunopathogenesis and immunogenetic variants in COVID-19
Pakorn Sagulkoo[SUP] 1 2 [/SUP], Kitiporn Plaimas[SUP] 3 4 [/SUP], Apichat Suratanee[SUP] 5 6 [/SUP], Andrea Name Colado Simão[SUP] 7 [/SUP], Edna Maria Vissoci Reiche[SUP] 7 [/SUP], Michael Maes[SUP] 8 9 10 [/SUP]
Affiliations
- PMID: 35598232
- DOI: 10.2174/1381612828666220519150821
Abstract
Coronavirus disease 2019 (COVID-19) continues to spread globally despite the discovery of vaccines. Many people die due to COVID-19 as a result of catastrophic consequences, such as acute respiratory distress syndrome, pulmonary embolism, and disseminated intravascular coagulation caused by a cytokine storm. Immunopathology and immunogenetic research may assist in diagnosing, predicting, and treating severe COVID-19 and the cytokine storm associated with COVID-19. This paper reviews the immunopathogenesis and immunogenetic variants that play a role in COVID-19. Although various immune-related genetic variants have been investigated in relation to severe COVID-19, the NOD-like receptor protein 3 (NLRP3) and interleukin 18 (IL-18) have not been assessed for their potential significance in the clinical outcome. Here, we a) summarize the current understanding of the immunogenetic etiology and pathophysiology of COVID-19 and the associated cytokine storm; and b) construct and analyze protein-protein interaction (PPI) networks (using enrichment and annotation analysis) based on the NLRP3 and IL18 variants and all genes, which were established in severe COVID-19. Our PPI network and enrichment analyses predict a) useful drug targets to prevent the onset of severe COVID-19 including key antiviral pathways such as Toll-Like-Receptor cascades, NOD-like receptor signaling, RIG-induction of interferon (IFN) α/β, and interleukin (IL)-1, IL-6, IL-12, IL-18, and tumor necrosis factor signaling; and b) SARS-CoV-2 innate immune evasion and the participation of MYD88 and MAVS in the pathophysiology of severe COVID-19. The PPI network genetic variants may be used to predict more severe COVID-19 outcomes, thereby opening the door for targeted preventive treatments.
Keywords: COVID-19; IL-18.; NLRP3; SARS-CoV-2; cytokines storm; inflammation; variant genotypes.