SARS-CoV-2 infection triggers pro-atherogenic inflammatory responses in human coronary [MAC_FOAM-RNAseq]

COVID-19 patients present higher risk for myocardial infarction (MI), acute coronary syndrome, and stroke for up to 1 year after SARS-CoV-2 infection. While the systemic inflammatory response to SARS-CoV-2 infection likely contributes to this increased cardiovascular risk, whether SARS35 CoV-2 directly infects the coronary vasculature and attendant atherosclerotic plaques to locally promote inflammation remains unknown. Here, we report that SARS-CoV-2 viral RNA (vRNA) is detectable and the virus replicates in coronary atherosclerotic lesions taken at autopsy from patients with severe COVID-19. Overall design: Human primary monocytes derived from PBMCs were obtained and differentiated to macrophages in the presence of 20 nM human macrophage-colony stimulating factor (M-CSF) for 5 days. Macrophages were first treated with ox-LDL at final concentration of 10 µg/mL for 1 hour before infection. Macrophages and foam cells were cultured with SARS-CoV-2 virus (USA-WA1/2020 strain) at MOI 0.1 in infection media with 2% FBS. Mock infected cells were used as controls. Cells were washed twice with PBS and harvested at different time points.