Our results indicate that various vital physiological pathways, including acute phase response signaling, cytokine and chemokine signaling, complement cascades, lipid transport and metabolism, and blood coagulation are modulated in Pf and Pv infections (Figure 4) . Alteration of the levels of several acute phase proteins (APPs) and multiple members of serum complement cascade as well as complement regulatory proteins (Table 2) due to the plasmodial infections is consistent with earlier findings [19] [20] [21] . Increased expression levels of circulating acute-phase amyloid proteins like serum amyloid A and P provide non-specific resistance against the pre-erythrocytic stages of Plasmodium, limit tissue damage and promote a rapid return to homeostasis [22, 23] . Interestingly, human serum paraoxonase (PON1) an HDLassociated esterase which protects lipoproteins against oxidation, found to be down-regulated in falciparum malaria patients. Acute inflammatory stimuli lead to reciprocal regulation of SAA and PON-1 [24] . Decreased serum PON-1 activity in context with falciparum malaria may in part be attributable to higher SAA level.