4. Modulation of the Inflammatory Phase
SARS-CoV-2 virus is capable of eliciting an immune reaction in the infected individual. Laboratory examinations have revealed that inflammatory factors such as interleukin (IL)-6, IL-1, IL-10 and tumour necrosis factor-α (TNFα) are upregulated during infection and can instigate an inflammatory response in the lower airways leading to lung injury in some instances (Conti et al., 2020; Guo et al., 2020). Additionally, in patients with severe symptoms of COVID-19, there may be activation of a cytokine storm, which can cause significant tissue damage (Mehta, McAuley, et al., 2020; Shi et al., 2020). A smaller proportion of patients can progress to a hyper-inflammatory state which in COVID-19 has been suggested to resemble secondary haemophagocytic lymphohistiocytosis (sHLH), a rare syndrome characterised by uncontrollable fever, cytopenia, raised ferritin levels and acute respiratory distress (Seguin, Galicier, Boutboul, Lemiale, & Azoulay, 2016). Interleukin and TNF-α levels show the greatest increase in those who require admission to the intensive care unit (ICU), suggesting that the cytokine storm is instrumental in severe COVID-19 cases (Huang et al., 2020). Therefore, there has been a logical progression towards the use of immunosuppressive agents as potential therapies to alleviate inflammation and hyperinflammation associated with COVID-19 (Mehta, McAuley, et al., 2020).