Under normal oxygen level (normoxia), HIF-1α is post-translationally hydroxylated by the prolyl hydroxylase domain enzymes (PHD) and subsequently undergoes proteasomal degradation.16,17 Hypoxia interferes with PHD-mediated degradation of HIF-1α, leading to stabilization of HIF-1α, heterodimerization with HIF-1β and subsequent activation of the HIF-1 pathway.17 Activation of HIF-1 plays multifaceted roles in infection-elicited inflammation. This evidence concerns the gene PDC and infection.