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].