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Infected red blood cells (iRBCs) evade spleen clearance by adhering to endothelial cells (ECs), triggering capillary blockage, inflammation, endothelial dysfunction and altered vascular permeability, prompting an endothelial transcriptional response. The iRBC<jats:sup>IT4var04<\/jats:sup>\/HBEC\u20105i model, where iRBCs present IT4var04 (VAR2CSA) on their surface, was used to analyze the effects of iRBC binding on ECs at different temperature (37\u00b0C vs. 40\u00b0C). Binding of non\u2010infected RBCs (niRBCs) and fever alone altered the expression of hundreds of genes in ECs. Comparing the expression profile of HBEC\u20105i cells cultured either in the presence of iRBCs or in the presence of niRBCs revealed significant upregulation of genes linked to immune response, nucleosome assembly, NF\u2010kappa B signaling, angiogenesis, and antiviral immune response\/interferon\u2010alpha\/beta signaling. Raising the temperature to 40\u00b0C, simulating fever, led to further upregulation of many genes, particularly those involved in cytokine production and angiogenesis. In summary, the presence of iRBCs stimulates ECs, activating several immunological pathways and affecting antiviral (\u2212parasitic) mechanisms and angiogenesis. 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