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.