As of March, 2023, over 6.8 million people have died from Coronavirus disease 2019 (COVID-19). The etiological agent of COVID-19 is Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2). SARS-CoV-2, one of the largest, positive sense RNA virus affects the lower and upper respiratory tract in humans leading to a severe acute respiratory syndrome. Severe cases of infection are characterized by a cascade of uncontrolled inflammatory responses by the host that lead to acute respiratory distress syndrome (ARDS), acute lung injury (ALI), compromised lung function, multiple-organ failure and eventually death. Studies have suggested that an intervention through regulation of the inflammatory response in COVID-19 patients could reduce disease-associated morbidity and mortality. More effective therapeutics are desperately needed. A better understanding of the molecular mechanisms involved in the dysregulation of host-response will facilitate the identification of targets and the development of effective therapeutics.
Patients with severe COVID-19 have elevated levels of proinflammatory cytokines, including IL-1b, IL-2, IL-6, IL-7, IL-8, TNF-a, CCL2, MIP-1a, and CXCL10. They also show an impaired IFN production along with downregulation of Interferon Stimulated Genes despite high virus load. Multiple viral proteins including Nsp1, Nsp13, Nsp14, membrane protein, spike protein, N protein, ORF3b, ORF6 and ORF8 have been reported to antagonize or dysregulate the IFN response. Potential modulators among the host factors include virus entry receptors, virus sensors, such as Toll Like Receptors, transcription factors and co-morbidities such as diabetes, coronary artery disease, renal disease, just to name a few. This Research Topic seeks to (i) gain molecular understanding underlying the dysregulation of inflammatory host response during SARS-CoV-2 infection; (ii) understand the dysregulation of host response through studies with viruses related to SARS-CoV-2; (iii) gain insights into potential therapeutic targets for the treatment of COVID-19; (iv) highlight potential therapeutic approaches to resolve COVID-19 and long COVID-19 syndrome.
We welcome Original Research articles, Methods, Reviews, Mini-reviews and Case Studies on the following sub-themes:
• molecular mechanism of SARS-CoV-2 mediated modulation of immune responses
• identification of novel viral or host factors involved in modulating antiviral immune response to SARS-CoV-2
• proposed approaches to target the inflammatory “cytokine storm” and IFN antagonism associated with SARS-CoV-2 infection
• mechanisms involved in Long COVID-19 syndrome
• studies on the immune response to viruses of the order Nidovirales, other than SARS-CoV-2.
Keywords:
Severe acute respiratory syndrome coronavirus 2, SARS-CoV-2, COVID-19, acute respiratory distress syndrome, acute lung injury, proinflammatory cytokines, IFN, interferon-stimulated genes
Important Note:
All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
As of March, 2023, over 6.8 million people have died from Coronavirus disease 2019 (COVID-19). The etiological agent of COVID-19 is Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2). SARS-CoV-2, one of the largest, positive sense RNA virus affects the lower and upper respiratory tract in humans leading to a severe acute respiratory syndrome. Severe cases of infection are characterized by a cascade of uncontrolled inflammatory responses by the host that lead to acute respiratory distress syndrome (ARDS), acute lung injury (ALI), compromised lung function, multiple-organ failure and eventually death. Studies have suggested that an intervention through regulation of the inflammatory response in COVID-19 patients could reduce disease-associated morbidity and mortality. More effective therapeutics are desperately needed. A better understanding of the molecular mechanisms involved in the dysregulation of host-response will facilitate the identification of targets and the development of effective therapeutics.
Patients with severe COVID-19 have elevated levels of proinflammatory cytokines, including IL-1b, IL-2, IL-6, IL-7, IL-8, TNF-a, CCL2, MIP-1a, and CXCL10. They also show an impaired IFN production along with downregulation of Interferon Stimulated Genes despite high virus load. Multiple viral proteins including Nsp1, Nsp13, Nsp14, membrane protein, spike protein, N protein, ORF3b, ORF6 and ORF8 have been reported to antagonize or dysregulate the IFN response. Potential modulators among the host factors include virus entry receptors, virus sensors, such as Toll Like Receptors, transcription factors and co-morbidities such as diabetes, coronary artery disease, renal disease, just to name a few. This Research Topic seeks to (i) gain molecular understanding underlying the dysregulation of inflammatory host response during SARS-CoV-2 infection; (ii) understand the dysregulation of host response through studies with viruses related to SARS-CoV-2; (iii) gain insights into potential therapeutic targets for the treatment of COVID-19; (iv) highlight potential therapeutic approaches to resolve COVID-19 and long COVID-19 syndrome.
We welcome Original Research articles, Methods, Reviews, Mini-reviews and Case Studies on the following sub-themes:
• molecular mechanism of SARS-CoV-2 mediated modulation of immune responses
• identification of novel viral or host factors involved in modulating antiviral immune response to SARS-CoV-2
• proposed approaches to target the inflammatory “cytokine storm” and IFN antagonism associated with SARS-CoV-2 infection
• mechanisms involved in Long COVID-19 syndrome
• studies on the immune response to viruses of the order Nidovirales, other than SARS-CoV-2.
Keywords:
Severe acute respiratory syndrome coronavirus 2, SARS-CoV-2, COVID-19, acute respiratory distress syndrome, acute lung injury, proinflammatory cytokines, IFN, interferon-stimulated genes
Important Note:
All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.