Host transcriptomic and histopathological evidence indicates that infection with the ΔsRNA0024 mutant suppresses amplification of the coagulation–complement and protease networks, dampens neutrophil recruitment and neutrophil extracellular trap (NET) formation, and lowers the burden on inflammation–metabolism signaling axes (PI3K–Akt, JAK–STAT, HIF-1/mTOR, AMPK), accompanied by contraction of ECM/adhesion and cytokine–receptor interaction modules. Here, SOAT1 is linked to infection.