Figure 3.

Viral infection and end organ damage. Increased redox stress drives viral replication, inflammation, apoptosis, vascular dysfunction and autoimmunity, in both acute infection with coronaviruses and in the setting of Post-Acute Sequelae of SARS-CoV-2 (PASC or Long COVID). Collectively, redox mediated pathways that drive viral replication, inflammation, apoptosis, autoimmunity, and vascular dysfunction contribute to cell and tissue damage that drives end organ disease in coronavirus infection. Cells enriched in mitochondria such as neurons, endothelial and epithelial cells may be particularly susceptible to increased redox stress driven by coronaviruses. Ultimately, increased redox stress during acute infection with coronaviruses and in the setting of PASC can directly or indirectly drive end organ disease such as brain, lung, liver, kidney and cardiovascular damage and induce intestinal dysfunction.