Fig. 2

Proposed model of protein interactions regulating PLTs roles in the pathogenesis of P. vivax infection. The figure depicts the protein–protein significant interactions found by STRING analysis (p-value < 0.05) with a high level of confidence (Score > 0.9). Protein names: PF4/CXCL4 (platelet factor 4); SERPINA 1 (Alpha 1 Anti-trypsin); SSA1 (serum amyloid A 1 protein); FERMT3 (Fermitin 3); TPM1 (Tropomyosin 1); ACTC1 (Actin, alpha cardiac muscle 1); MYL12B (Myosin regulatory light chain 12B); MYL6 (Myosin light chain 6); MYH9 (Myosin heavy chain 9); GP5/V (Glycoprotein 5/V); RAP1B; VWf (Von Willebrand Factor). The lines depict the level of interaction evidence (Purple: experimental; gray: curated databases; blue: gene co-occurrence; black: co-expression). Even though VWf was not found differentially regulated in platelet proteomes, VWf plasma levels were higher in P. vivax patients (Fig. 3), thus it was included in the interactome to analyze its relationship with the most important differentially regulated PLT proteins (Red arrow). The black arrow depicts the protein GPV significantly decreased in the T-Pv group