About this Research Topic
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
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