Endothelial activation and dysfunction in severe fever with thrombocytopenia syndrome.

Abstract:

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 1.1×107 pg/mL SAA-1 or 1.2×106 pg/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.

journal_name

PLoS Negl Trop Dis

authors

Li XK,Yang ZD,Du J,Xing B,Cui N,Zhang PH,Li H,Zhang XA,Lu QB,Liu W

doi

10.1371/journal.pntd.0005746

subject

Has Abstract

pub_date

2017-08-14 00:00:00

pages

e0005746

issue

8

eissn

1935-2727

issn

1935-2735

pii

PNTD-D-17-00095

journal_volume

11

pub_type

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