likely infect CD68+ macrophages and dendritic cells initially, although the ultimate targets are endothelial cells; TLR4 is important for recognition with initial infection and animals deficient in this signaling pathway are more susceptible to infection, and infection can alter transcriptional programs in these cells to potentially benefit propagation and influence disease severity; disease results from both direct effects of the pathogen on critical vascular barriers in organs and the ensuing inflammatory responses. This evidence concerns the gene TLR4 and infection.