By Max De La Cruz Morrobel, Katriana Meiman

Faculty Mentor: Dr. Laura Sipe

Abstract

After infection, SARS-CoV-2 can leave patients with long-term inflammatory cytokine release and connective tissue damage. Studies suggest that this is due to viral infection inhibiting oxidative phosphorylation in macrophages, polarizing them into the inflammatory M1 phenotype and releasing an extracellular-matrix cleaving enzyme Matrix Metalloprotease-2 (MMP-2). To simulate post-viral infection on macrophages, we assessed inflammatory activity of RAW 264.7 macrophages treated with inflammatory lipopolysaccharide (LPS) and/or the electron transport chain inhibitor antimycin A and tested for the inflammatory markers Nitric Oxide (NO) and Tumour Necrosis Factor-α (TNF-a). A Griess reagent assay showed a slight enhancement of LPS stimulated NO release following antimycin A treatment. However, an ELISA showed that antimycin A did not impact TNF-a release. Neither treatment impacted cellular respiration. These findings suggest that SARS-CoV-2 does not cause excessive cytokine release and connective tissue damage through prolonged inhibition of oxidative phosphorylation. Future directions include inhibiting other areas of oxidative phosphorylation and assessing MMP-2 levels.