scholarly journals Human Polyomavirus 7-Associated Pruritic Rash and Viremia in Transplant Recipients

2014 ◽  
Vol 211 (10) ◽  
pp. 1560-1565 ◽  
Author(s):  
J. Ho ◽  
J. J. Jedrych ◽  
H. Feng ◽  
A. A. Natalie ◽  
L. Grandinetti ◽  
...  
2005 ◽  
Vol 79 (22) ◽  
pp. 14442-14445 ◽  
Author(s):  
Aisling S. Dugan ◽  
Sylvia Eash ◽  
Walter J. Atwood

ABSTRACT BK virus (BKV) is a common human polyomavirus infecting >80% of the population worldwide. Infection with BKV is asymptomatic, but reactivation in renal transplant recipients can lead to polyomavirus-associated nephropathy. In this report, we show that enzymatic removal of α(2,3)-linked sialic acid from cells inhibited BKV infection. Reconstitution of asialo cells with α(2,3)-specific sialyltransferase restored susceptibility to infection. Inhibition of N-linked glycosylation with tunicamycin reduced infection, but inhibition of O-linked glycosylation did not. An O-linked-specific α(2,3)-sialyltransferase was unable to restore infection in asialo cells. Taken together, these data indicate that an N-linked glycoprotein containing α(2,3)-linked sialic acid is a critical component of the cellular receptor for BKV.


2019 ◽  
Vol 120 ◽  
pp. 6-11 ◽  
Author(s):  
Yilin Wang ◽  
Robert Strassl ◽  
Ilkka Helanterä ◽  
Stephan W. Aberle ◽  
Gregor Bond ◽  
...  

Intervirology ◽  
2004 ◽  
Vol 47 (1) ◽  
pp. 41-47 ◽  
Author(s):  
Chiara Merlino ◽  
Massimiliano Bergallo ◽  
Franca Giacchino ◽  
Roberta Daniele ◽  
Christian Bollero ◽  
...  

Blood ◽  
2011 ◽  
Vol 118 (21) ◽  
pp. 3223-3223
Author(s):  
Francesca Lorraine Wei Inng Lim ◽  
Ai Ling Teo ◽  
Yvonne SM Loh ◽  
William YK Hwang ◽  
Yeow-Tee Goh ◽  
...  

Abstract Abstract 3223 Abstract The human polyomavirus type 1, better known as “BK virus” (BKV), persists in a latent state in more than 90% of the world's population. It is infamous as a pathogen in kidney transplant recipients by causing BKV-associated nephropathy (BKVN) often resulting in allograft dysfunction and loss. BKV has also been associated with hemorrhagic cystitis (HC) in haematopoietic stem cell transplant (HSCT) recipients. However, treatment for this condition remains challenging, as the mechanism through which BKV reactivation causes HC in HSCT recipients is not known. In addition, there is currently little data about the reconstitution of BKV-specific immunity after HSCT and its relationship to HC. It is still unclear whether the BKV-specific T cell response helps to prevent and bring about the resolution of HC, or if HC is an immunopathology and the BKV specific immunity damages the bladder mucosa in the process of attacking BKV-infected urothelial cells. We hypothesized that BKV-associated HC is initiated by an imbalance between immune surveillance and BKV reactivation, followed by eventual rebound of BKV- specific T immunity causing an immunopathological reaction towards BKV-infected urothelial cells that ultimately lead to cystitis after HSCT. We aim to correlate BKV titre levels in the urine and blood with BKV- specific T cells. This is a novel prospective study that describes the immune reconstitution of BKV specific T cells immunity after allogeneic HSCT and uses the clinical manifestation of HC as a maker to analyze reconstitution of the immune system post HSCT. This study was approved by the institutional review board. Ten patients undergoing allogeneic HSCT were recruited over a 1 year period. The clinical data collected included conditioning regime, indication for transplant, presence of GVHD and development of HC. Patient's blood samples were collected prior to conditioning and at 4 weekly intervals for 24 weeks. Peripheral blood mononuclear cells (PBMCs) isolated from these whole blood samples were then stimulated with overlapping peptide mixes of BK LT and VP1. Quantification of BKV-specific T cells were accomplished by flow cytometry. Results revealed higher levels of CD3+IL-17+BKV specific T cells (p<0.05) in subjects who developed HC compared to those who did not. Peak levels of CD3+IL-17+BKV specific T cells were observed just before or just after the presentation of HC. Both CD4+IL-17+ (p<0.01) and CD8+IL-17+ (p=0.05) BKV specific T cells were significantly higher in patients who developed HC compared to those who did not. This increment of IL-17+ BKV-specific T immune cells coincided with high levels of BKV detected in the urine. These preliminary results strongly suggest that BKV-associated HC is an immunopathology caused by IL-17 secreting BKV-specific T cells. Though our cohort of patients is small however in view of the promising results; we plan to extend the study to a larger cohort of patient. The demonstration of an immunological basis of HC will provide a theoretical framework for the development of potential immunotherapeutic interventions in the prevention and treatment of HC. Disclosures: No relevant conflicts of interest to declare.


2012 ◽  
Vol 93 (4) ◽  
pp. 698-705 ◽  
Author(s):  
Franziska Trusch ◽  
Marcus Klein ◽  
Tim Finsterbusch ◽  
Joachim Kühn ◽  
Jörg Hofmann ◽  
...  

Human polyomavirus 9 (HPyV9) was discovered recently in immunocompromised patients and shown to be genetically closely related to B-lymphotropic polyomavirus (LPyV). No serological data are available for HPyV9, but human antibodies against LPyV have been reported previously. To investigate the seroepidemiology of HPyV9 and the sero-cross-reactivity between HPyV9 and LPyV, a capsomer-based IgG ELISA was established using the major capsid protein VP1 of HPyV9 and LPyV. VP1 of an avian polyomavirus was used as control. For HPyV9, a seroprevalence of 47 % was determined in healthy adults and adolescents (n = 328) and 20 % in a group of children (n = 101). In both groups, the seroreactivities for LPyV were less frequent and the ELISA titres of LPyV were lower. Of the HPyV9-reactive sera, 47 % reacted also with LPyV, and the titres for both PyVs correlated. Sera from African green monkeys, the natural hosts of LPyV, reacted also with both HPyV9 and LPyV, but here the HPyV9 titres were lower. This potential sero-cross-reactivity between HPyV9 and LPyV was confirmed by competition assays, and it was hypothesized that the reactivity of human sera against LPyV may generally be due to cross-reactivity between HPyV9 and LPyV. The HPyV9 seroprevalence of liver transplant recipients and patients with neurological dysfunctions did not differ from that of age-matched controls, but a significantly higher seroprevalence was determined in renal and haematopoietic stem-cell transplant recipients, indicating that certain immunocompromised patient groups may be at a higher risk for primary infection with or for reactivation of HPyV9.


2004 ◽  
Vol 78 (21) ◽  
pp. 11583-11590 ◽  
Author(s):  
Sylvia Eash ◽  
William Querbes ◽  
Walter J. Atwood

ABSTRACT Polyomavirus-associated nephropathy occurs in ∼5% of renal transplant recipients and results in loss of graft function in 50 to 70% of these patients. The disease is caused by reactivation of the common human polyomavirus BK (BKV) in the transplanted kidney. The early events in productive BKV infection are unknown. In this report, we focus on elucidating the mechanisms of BKV internalization in its target cell. Our data reveal that BKV entry into permissive Vero cells is slow, is independent of clathrin-coated-pit assembly, is dependent on an intact caveolin-1 scaffolding domain, is sensitive to tyrosine kinase inhibition, and requires cholesterol. BKV colocalizes with the caveola-mediated endocytic marker cholera toxin subunit B but not with the clathrin-dependent endocytic marker transferrin. In addition, BKV infectious entry is sensitive to elevation in intracellular pH. These findings indicate that BKV entry into Vero cells occurs by caveola-mediated endocytosis involving a pH-dependent step.


2001 ◽  
Vol 120 (5) ◽  
pp. A562-A562
Author(s):  
A HABIB ◽  
B BACON ◽  
S RAMRAKHIANI

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