| Abstract | Since January 10, 2020, when the first death linked to the severe acute respiratory syndrome-related coronavirus 2 (SARS-CoV-2) occurred in Wuhan, China, more than 530,000 people have died (as of July 4, 2020). Globally, there are 11.2 million people infected with the virus, with 2.9 million in the USA alone and other populous countries surging. While there is a charge to develop a vaccine, as well as means of eliminating the virus from those infected (e.g., remdesivir), neither of these therapeutic strategies will directly address the major life-threatening complications that may occur once infected, namely, the profound upregulation of the innate immune system. Like the severe acute respiratory syndrome coronavirus that emerged in 2002 (SARS-1, caused by SARS-CoV) and the Middle East respiratory syndrome-related coronavirus of 2012 (MERS-CoV), COVID-19 (the disease associated with SARS-CoV-2) is associated with a storm of pro-inflammatory cytokines like IL-1β, IL-6, and TNF. Precisely why some patients evolve to this hyper-inflammation state while others do not remains unclear but is likely due to nonviral factors that are specific to the host, including age and comorbidities (Yang et al. 2020). These cytokines play an important role in various tissue complications with acute respiratory distress syndrome (ARDS), a form of acute lung injury that is without tangible therapeutic options apart from supportive care, of principal concern (Nieto-Torres et al. 2015). |
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