scholarly journals Adenovirus coxsackie adenovirus receptor-mediated binding to human erythrocytes does not preclude systemic transduction

2016 ◽  
Vol 23 (12) ◽  
pp. 411-414 ◽  
Author(s):  
L A Rojas ◽  
R Moreno ◽  
H Calderón ◽  
R Alemany
Keyword(s):  
Human Erythrocytes ◽  
Coxsackie Adenovirus Receptor ◽  
Adenovirus Receptor

Adenovirus-induced thrombocytopenia: the role of von Willebrand factor and P-selectin in mediating accelerated platelet clearance

Blood ◽  
2006 ◽  
Vol 109 (7) ◽  
pp. 2832-2839 ◽  
Author(s):  
Maha Othman ◽  
Andrea Labelle ◽  
Ian Mazzetti ◽  
Hisham S. Elbatarny ◽  
David Lillicrap
Keyword(s):  
Von Willebrand Factor ◽  
Cell Activation ◽  
Endothelial Cell Activation ◽  
Platelet Surface ◽  
Adenoviral Gene Transfer ◽  
Coxsackie Adenovirus Receptor ◽  
Transfer Vectors ◽  
Adenovirus Receptor ◽  
Von Willebrand ◽  
Willebrand Factor

AbstractThrombocytopenia has been consistently reported following the administration of adenoviral gene transfer vectors. The mechanism underlying this phenomenon is currently unknown. In this study, we have assessed the influence of von Willebrand Factor (VWF) and P-selectin on the clearance of platelets following adenovirus administration. In mice, thrombocytopenia occurs between 5 and 24 hours after adenovirus delivery. The virus activates platelets and induces platelet-leukocyte aggregate formation. There is an associated increase in platelet and leukocyte-derived microparticles. Adenovirus-induced endothelial cell activation was shown by VCAM-1 expression on virus-treated, cultured endothelial cells and by the release of ultra-large molecular weight multimers of VWF within 1 to 2 hours of virus administration with an accompanying elevation of endothelial microparticles. In contrast, VWF knockout (KO) mice did not show significant thrombocytopenia after adenovirus administration. We have also shown that adenovirus interferes with adhesion of platelets to a fibronectin-coated surface and flow cytometry revealed the presence of the Coxsackie adenovirus receptor on the platelet surface. We conclude that VWF and P-selectin are critically involved in a complex platelet-leukocyte-endothelial interplay, resulting in platelet activation and accelerated platelet clearance following adenovirus administration.

The endosomal epsilon-coatomer protein is involved in human adenovirus type 5 internalisation

2002 ◽  
Vol 50 (4) ◽  
pp. 481-489 ◽  
Author(s):  
Cs. Jeney ◽  
Boglárka Banizs ◽  
Orsolya Dobay ◽  
Keyword(s):  
Chinese Hamster ◽  
Human Adenovirus ◽  
Adenovirus Type ◽  
Inhibitory Effect ◽  
Bafilomycin A1 ◽  
Cho Cell ◽  
Coxsackie Adenovirus Receptor ◽  
Downstream Effector ◽  
Adenovirus Receptor ◽  
Adenovirus Type 5

The effects of bafilomycin A1 and of the reduced level of endosomal epsilon-COP (coatomer protein) on the infectivity of human adenovirus type 5 were investigated in Coxsackie adenovirus receptor- (CAR-) transfected Chinese hamster ovary (CHO) cells. The endosomal proton pump inhibitor bafilomycin A1 was able to cause only partial inhibition. Using ldlF cells (an epsilon-COP thermosensitive mutant CHO cell line) the reduction of epsilon-COP level also had partial inhibitory effect. Based on these results and comparing them to existing models of the adenovirus entry, we propose a refined model in which there are two pathways of adenoviral entry: the first one involves the epsilon-COP as the downstream effector of the acidification and can be blocked by bafilomycin A1 and the second one is a pH-independent pathway.

scholarly journals Spliceform specific Coxsackie‐adenovirus receptor interactions

2008 ◽  
Vol 22 (S1) ◽  
Author(s):  
Katherine Ashbourne Excoffon ◽  
Nicholas Gansemer ◽  
Joseph Zabner
Keyword(s):  
Coxsackie Adenovirus Receptor ◽  
Receptor Interactions ◽  
Adenovirus Receptor

scholarly journals More recent swine vesicular disease virus isolates retain binding to coxsackie–adenovirus receptor, but have lost the ability to bind human decay-accelerating factor (CD55)

2005 ◽  
Vol 86 (5) ◽  
pp. 1369-1377 ◽  
Author(s):  
Miguel A. Jimenez-Clavero ◽  
Estela Escribano-Romero ◽  
Victoria Ley ◽  
O. Brad Spiller
Keyword(s):  
Cell Line ◽  
Disease Virus ◽  
Hela Cells ◽  
Virus Titre ◽  
Decay Accelerating Factor ◽  
Coxsackie Adenovirus Receptor ◽  
Swine Vesicular Disease Virus ◽  
Virus Serotype ◽  
Adenovirus Receptor ◽  
Vesicular Disease

Swine vesicular disease virus (SVDV) evolved from coxsackie B virus serotype 5 (CVB5) in the recent past, crossing the species barrier from humans to pigs. Here, SVDV isolates from early and recent outbreaks have been compared for their capacity to utilize the progenitor virus receptors coxsackie–adenovirus receptor (CAR) and decay-accelerating factor (DAF; CD55). Virus titre of CVB5 and SVDV isolates It′66 and UK′72 on human HeLa cells was reduced by pre-incubation with either anti-DAF or anti-CAR antibodies; however, recent SVDV isolates R1072, R1120 and SPA′93 did not infect HeLa cells lytically. CVB5 and SVDV infection of the pig cell line IB-RS-2 was inhibited completely by anti-CAR antibodies for all isolates, and no reduction was observed following pre-incubation of cells with anti-pig DAF antibodies. Expression of human DAF in the pig cell line IB-RS-2 enhanced the virus titre of early SVDV isolates by 25-fold, but had no effect on recent SVDV isolate titre. Binding of radiolabelled CVB5 to IB-RS-2 cells was increased seven- to eightfold by expression of human DAF and binding of early SVDV isolates was increased 1·2–1·3-fold, whereas no increase in binding by recent SVDV isolates was mediated by human DAF expression. Addition of soluble hDAF-Fc inhibited CVB5, but not SVDV, infection of pig cells. Pre-incubation of all viruses with soluble hCAR-Fc blocked infection of IB-RS-2 pig cells completely; titration of the amount of soluble hCAR-Fc required to block infection revealed that early isolate UK′72 was the least susceptible to inhibition, and the most recent isolate, SPA′93, was the most susceptible.

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