Introduction
Coronavirus infection is typically associated with mild clinical symptoms, save for those due to infection with severe acute respiratory syndrome coronavirus (SARS-CoV)1, the Middle East respiratory syndrome coronavirus (MERS-CoV)2, 3, and most recently, with SARS-CoV-2. An understanding of the pathophysiology of SARS-CoV-associated pneumonia induced will be helpful toward understanding the disease associated with the novel SARS-CoV-2 pathogen, a severe pneumonia known as Coronavirus Disease 2019 (2019-nCoV or COVID-19). Most of the published reports indicate that fatal COVID-19 has a clinical presentation that resembles that due to the original 2003 SARS-CoV pathogen. Most notably, in both cases, synthesis and release of proinflammatory cytokines has been associated with disease severity. Ongoing production can result in a cytokine storm and acute respiratory distress syndrome which are findings that can lead to fatal disease4. Toll-like receptors (TLRs), NF-κB, macrophages, and proinflammatory cytokines were all found to be involved in the development of severe pneumonia5.