- SARS-Cov-2 infection produce reactive oxygen species (ROS)
- ROS induce HIF1a (hypoxia induced Factor-1a)
- HIF1a induce transcription of proinflammatory cytokines
- Increased PD-1, IL-1, IL-6, TNFa
- Decreases anti-inflammatory cytokines 
- Decreased IFNg
- Increases epithelial cell death
- Decreased T cell proliferation

SARS-CoV-2 induces cytokine storm

During SARS-CoV-2 infection, elevated glucose levels and sustained aerobic glycolysis in monocytes directly promote viral replication, cytokine production, T cell dysfunction, and lung epithelial cell death.

Northwestern University

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COVID-19 is more severe in Diabetic people


Elevated Glucose Levels Favor SARS-CoV-2 Infection and Monocyte Response through a HIF-1α/Glycolysis-Dependent Axis

Targeting metabolic pathways may provide new therapeutic strategies to treat COVID-19.

Targeting Metabolic Pathways for COVID-19 Treatment

Obese and diabetic individuals typically exhibit uncontrolled blood glucose levels, which are associated with a greater risk of developing severe COVID-19 infection. SARS-CoV-2 infection in these patients may trigger a cytokine storm, potentially driven by a dysfunctional adaptive immune response and epithelial cell death.

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