Cytokine release syndrome in severe COVID-19
By J. B. Moore, C. June. Science, 2020
1,792 citations recorded by the source corpus.
Lessons from arthritis and cell therapy in cancer patients point to therapy for severe disease In December 2019, a new strain of coronavirus, severe acute respiratory syndrome–coronavirus 2 (SARS-CoV-2), was recognized to have emerged in Wuhan, China. Along with SARS-CoV and Middle East respiratory syndrome–coronavirus (MERS-CoV), SARS-CoV-2 is the third coronavirus to cause severe respiratory illness in humans, called coronavirus disease 2019 (COVID-19). This was recognized as a pandemic by the World Health Organization (WHO) in March 2020 and has had considerable global economic and health impacts. Although the situation is rapidly evolving, severe disease manifested by fever and pneumonia, leading to acute respiratory distress syndrome (ARDS), has been described in up to 20% of COVID-19 cases. This is reminiscent of cytokine release syndrome (CRS)–induced ARDS and secondary hemophagocytic lymphohistiocytosis (sHLH) observed in patients with SARS-CoV and MERS-CoV as well as in leukemia patients receiving engineered T cell therapy. Given this experience, urgently needed therapeutics based on suppressing CRS, such as tocilizumab, have entered clinical trials to treat COVID-19.
Subfields: Hematology, Infectious Diseases, Neurology
View Paper: https://www.semanticscholar.org/paper/187405e10abec17d9e7f65e9315056039815b7b3
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Citations in the corpus
- More Than 50 Long-Term Effects of COVID-19: A Systematic Review and Meta-Analysis (2021, neutral): “5 (19-84) 63 Fatigue, dyspnea, joint pain, chest pain, cough, anosmia, Sicca syndrome, Rhinitis, red eyes, dysgeusia, headache, sputum, lack of appetite, sore throat, vertigo, myalgia, diarrhea.”
- Deep immune profiling of COVID-19 patients reveals distinct immunotypes with therapeutic implications (2020, background): “A key feature of COVID-19 is thought to be an inflammatory response that, at least in some patients, is linked to clinical disease manifestation (2, 4) and high levels of chemokines and cytokines, including IL-1RA, IL-6, IL-8, IL-10, and CXCL10 (11, 41).”
- IL-6 in inflammation, autoimmunity and cancer (2020, background): “Therefore, SARS-CoV-1 and SARS-CoV-2 infection activate both NF-κ B and STAT3, key elements of the IL-6 Amp, to cause cytokine storm (12, 13, 15, 349, 350).”
- The cytokine storm and COVID‐19 (2020, background): “TCZ binds to both mIL‐6R and sIL‐6R and inhibits both cis‐ and trans‐signaling and trans‐presentation.(40,65) Of note, IL‐6 inhibitors are not able to bind to IL‐6 produced by viruses such as HIV and human herpesvirus‐8.”
- Immunology of COVID-19: Current State of the Science (2020, neutral): “Following preliminary reports of IL-6 as a critical cytokine in COVID-19-associated CRS, monoclonal antibodies that target the IL-6 signaling pathway have been proposed as therapeutic candidates (Moore and June, 2020) (Figure 6C).”
- Dexamethasone in Hospitalized Patients with Covid-19 (2021, neutral): “Unknown 190 (9) 399 (9) 123 (8) 327 (8) 139 (14)”
- Effect of Dexamethasone in Hospitalized Patients with COVID-19: Preliminary Report (2020, background): “Inflammatory organ injury may occur in severe COVID-19, with a subset of patients having markedly elevated inflammatory markers such as C-reactive protein, ferritin, and interleukins 1 and 6.(6,15,16) Several therapeutic interventions to mitigate inflammatory organ injury have been proposed in viral”