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Deprecated: Implicit conversion from float 300.79999999999995 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 J+Infect+Dis 2018 ; 217 (3): 456-465 Nephropedia Template TP
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Human Parvovirus B19 (B19V) Up-regulates CXCR4 Surface Expression of Circulating Angiogenic Cells: Implications for Cardiac Ischemia in B19V Cardiomyopathy #MMPMID28961998
J Infect Dis 2018[Jan]; 217 (3): 456-465 PMID28961998show ga
BACKGROUND: Human parvovirus B19 (B19V) infection and damage of circulating angiogenic cells (CAC) results in dysfunctional endogenous vascular repair (DEVR) with secondary end-organ damage. Trafficking of CAC is regulated by SDF-1alpha and the respective receptor CXCR4. We thus tested the hypothesis of a deregulated CXCR4/SDF-1alpha axis in symptomatic B19V-cardiomyopathy. METHODS: CAC were infected in vitro with B19V and transfected with B19V-components. Read-out were: CXCR4-expression and migratory capacity at increasing doses of SDF-1alpha. In 31 patients with chronic B19V-cardiomyopathy compared to 20 controls read-outs were from blood: migratory capacity, CXCR4 expression on CAC, serum SDF-1alpha; from cardiac biopsies: SDF-1alpha mRNA, HIF-1alpha mRNA, microvascular density, resident cardiac stem cells (CSC), transcardiac gradients of CAC. RESULTS: In vitro B19V-infected CAC showed up-regulation of surface CXCR4 with increased migratory capacity further enhanced by elevated SDF-1alpha concentrations. Overexpression of the B19V capsid protein VP2 was associated with this effect. Chronic B19V-cardiomyopathy patients showed increased numbers of ischaemia mobilised CAC but DEVR as well as diminished numbers of CAC after transcardiac passage. Cardiac microvascular density and CSC were significantly reduced in B19V-cardiomyopathy. CONCLUSIONS: We thus conclude that B19V infection has a direct VP2-mediated negative impact on trafficking of CAC in the presence of impaired cardiac regeneration.