This could be due to 1) T. gondii suppression of these host responses and/or 2) direct induction of a more dramatic host response during infection by H. hammondi. Since IFNγ-signaling is critical for controlling T. gondii infection [30–32] we examined all members of the interferon signaling pathway and identified a subset of them (BAK1, 1FITM1, 1FITM2, JAK1, JAK2 and PSMB8) that were of significantly higher abundance in H. hammondi-infected THP-1 cells but were comparatively unchanged during infection with T. gondii (S2B Fig). Here, BAK1 is linked to infection.