Endothelial activation and dysfunction in severe fever with thrombocytopenia syndrome

Background: pathogenesis of severe fever with thrombocytopenia syndrome (sfts) has not been well described yet. recent studies indicate that sftsv could replicate in endothelial cells. here we performed a case-control study to determine whether endothelial activation/dysfunction occurred in sftsv infection and to identify the biomarkers reflecting endothelial dysfunction. methodology/principal findings: in a case-control study of 134 sfts patients and 68 healthy controls,serum levels of plasminogen activator inhibitor 1,tissue plasminogen activator,p-selectin,platelet endothelial cell adhesion molecular,cd40 ligand,e-selectin,vascular endothelial growth factor a,serum amyloid antigen 1 (saa-1) and vascular cell adhesion molecular 1 were significantly enhanced in the patients than the controls (all p<0.05),indicating the occurrence of endothelial activation/dysfunction in sfts. the intercellular adhesion molecular 1 (icam-1) and saa-1 at the convalescent phase were also significantly associated with severe patients,after adjusting for the potential confounders. the odds ratio was estimated to be 3.364 (95% ci 1.074–10.534) for icam-1,and 1.881 (95% ci 1.166–3.034) for saa-1,respectively. cutoff value of 1.1×107pg/ml saa-1 or 1.2×106pg/ml icam-1 were found to have moderate power of predicting fatal cases. conclusions: the endothelial dysfunction may be one of the pathogenic mechanism of sfts. the serum levels of icam-1 and saa-1 might be used to predict adverse outcome. © 2017 li et al.