Data for 'Risk factors for severe COVID-19 disease increase SARS CoV-2 infectivity of endothelial cells and pericytes'

Data for paper published in Open Biology (12/06/2024)
Each .csv file is the data for a different figure or sub-figure, as indicated in the file name. All data is viral titre in different cells in response to incubation with SARS CoV-2 pseudo-typed virus (PV). The cells, genotype, type of PV and other experimental variables are listed in column headers.
Matching R markdown code to use these data to generate the figures in the linked manuscript are provided. These can be used by saving all the data files into a folder, from which there is a subfolder called "Analysis". The R code will then generate the figures and save analyses into that subfolder.
AbstractCOVID-19 was initially considered a primarily respiratory disease but is now known to affect other organs including the heart and brain. A major route by which COVID-19 impacts different organs is via the vascular system. We studied the impact of apolipoprotein E (APOE) genotype and inflammation on vascular infectivity by pseudo-typed SARS-CoV-2 viruses in mouse and human cultured endothelial cells and pericytes. Possessing the APOE4 allele or having existing systemic inflammation is known to enhance the severity of COVID-19. Using targeted replacement human APOE3 and APOE4 mice, and inflammation induced by bacterial lipopolysaccharide (LPS) we investigated infection by SARS-CoV-2. Here, we show that infectivity was higher in murine cerebrovascular pericytes compared to endothelial cells, and higher in cultures expressing APOE4. Furthermore, increasing the inflammatory state of the cells by prior incubation with LPS increased infectivity into human and mouse pericytes, and human endothelial cells. Our findings provide insights into the mechanisms underlying severe COVID-19 infection, highlighting how risk factors such as APOE4 genotype and prior inflammation may exacerbate disease severity by augmenting the virus's ability to infect vascular cells.