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Cytokine storms have been shown to be common pathologies in severe SARS-CoV-2 infections.
Updated June 29, 2022
The pathologies and symptoms of COVID-19 have been shown to be highly heterogeneous, with many of the immunological determinants of disease progression and prognosis still unknown. Severe cases of COVID-19 typically present with high viral loads, respiratory distress, and pulmonary damage that correlate with increases in cytokine levels. Termed cytokine storm syndrome (CSS), excessive cytokine release is a key driver of the acute respiratory distress syndrome (ARDS), which is thought to be the leading cause of COVID-19 mortality1.
For an overview of immune cell signaling and cytokine targets, download our interactive poster.
Download cytokine storm in COVID-19 poster.
Cytokines coordinate the body's response to infection and damage, triggering inflammation. However, in some cases, cytokines can be released in excessive or uncontrolled amounts, causing harm to the body. Cytokine storm syndromes can lead to vital organ failure, including of the cardiac, lung and renal systems, and result in death. Initial evidence from China demonstrated elevated levels of the cytokines IL-6, IL-2R, CRP and ferritin in severe cases of SARS-CoV-2 infection2-4. Further studies have since highlighted persistently raised levels of many additional cytokines, including TNF-alpha, IP-10, MCP-3, and IL-1RA in severe cases4, 5.
Researchers are analyzing potential treatments for the cytokine storm response seen in patients, of which dexamethasone has been shown as to be a cost-effective treatment. An alternative approach may be through targeting tumor necrosis factor-alpha (TNF-alpha)6: an important cytokine in nearly all acute inflammatory reactions and a frequently elevated biomarker in the blood and tissues of COVID-19 patients7. Other targets that have been under investigation include TLR4, IFN, IL1, IL6, and CSF.
For an overview of the cytokine response in COVID-19 download our poster.
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References