Pathogenesis of CSS
The pathogenesis of CSS has not been fully known. Several studies have shown that the mechanism of CSS depends on the imbalance of pro-inflammatory and anti-inflammatory process and the interaction of specific cells and cytokines, resulting in immune regulation disorder. Cytokines can be markedly increased in patients with CSS, which differ according to the heterogeneity of the disease. A previous study found that H5N1 infected patients had higher levels of interferon-gamma-induced protein-10 (IP-10), monocyte chemoattractant protein 1 (MCP-1) and IL-8 than patients with seasonal H1N1 influenza [6]. Moreover, it was confirmed that cytokines play an important role in the pathogenesis of severe CoV infection. The proinflammatory cytokines (IFN-γ, IL-1, IL-6, IL-12, transforming growth factor-β (TGF-β)) in severe SARS patients’ sera were significantly higher than those with mild to moderate symptoms. Also, in severe MERS patients, serum inflammatory cytokines (IFN-α, IL-6, IL-8) were significantly increased [7].