These data, together with the extensive framework of hepatic vacuolization and accumulation of lipids in the liver, suggested that the infection with T. gondii in the absence of CCR5 may have led to the block or a to lack of activation of some metabolic pathways involving peroxisome or mitochondria, responsible for β-oxidation or lipid neogenesis, induced by PPARα. Here, CCR5 is linked to infection.