Coronavirus disease 2019 (COVID-19) is a worldwide health crisis due to infection by the severe acute respiratory syndrome corona virus-2 (SARS-CoV-2). Severe COVID-19 is characterized by hypoxia, inflammation, pneumonia, and hypercoagulability. Studies suggest that COVID-19 patients are at high risk of clotting events. Other complications such as renal failure and neurological abnormalities may be due to microvascular thrombosis, and may contribute to poor patient outcomes. Proteomic and metabolomic profiling of blood from COVID-19 patients identified alterations in metabolic and complement pathways that suggest dysregulated immunomodulation, hypercoagulation, and oxygen transport and availability. Illness severity, underlying conditions, and SARS-CoV-2 infection may all contribute to these alterations and ongoing studies will help in understanding these interactions. This session describes the altered metabolic pathways and altered hemostasis that may influence disease severity.
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Describe how metabolomic, lipidomic, and proteomic profiling of blood is useful for identifying dysregulated pathways associated with COVID-19 that potentially contribute to severe disease.
Identify how metabolic changes in red blood cells modulate oxygen transport and availability in general, with possible applications to patients with COVID-19.
Identify mechanisms that contribute to hypercoagulability in patients with COVID-19.