crucial to ensure the best outcome for recovery, allowing treatment with a variety of biological agents that target the cytokines to reduce their levels. Meta-analysis suggests clear patterns distinguishing patients with or without severe disease. Possible predictors of severe and fatal cases may include "lymphopenia, thrombocytopenia and high levels of ferritin, D-dimer, aspartate aminotransferase, lactate dehydrogenase, C-reactive protein, neutrophils, procalcitonin and creatinine" as well as interleukin-6 (IL-6). Ferritin and IL-6 are considered to be possible immunological biomarkers for severe and fatal cases of COVID-19. Ferritin and C-reactive protein may be possible screening tools for early diagnosis of systemic inflammatory response syndrome in cases of COVID-19. Due to the increased levels of cytokines and interferons in patients with severe COVID-19, both have been investigated as potential targets for SARS-CoV-2 therapy. An animal study found that mice producing an early strong interferon response to SARS-CoV-2 were likely to live, but in other cases the disease progressed to a highly morbid overactive immune system. The high mortality rate of COVID-19 in older populations has been attributed to the impact of age on interferon responses. Short-term use of dexamethasone, a synthetic corticosteroid, has been demonstrated to reduce the severity of inflammation and lung damage induced by a cytokine storm by inhibiting the severe cytokine storm or the hyperinflammatory phase in patients with COVID-19. Clinical trials continue to identify causes of cytokine storms in COVID-19 cases. One such cause is the delayed Type I interferon response that leads to accumulation of pathogenic monocytes. High viremia is also associated with exacerbated Type I interferons response and worse prognosis. Diabetes, hypertension, and cardiovascular disease are all risk factors of cytokine storms in COVID-19 patients. References Immunology Endocrine system