Abstract

The frequency of B19 infection in renal transplant donors and recipients was studied to determine the significance of active viral infection in the development of anemia. Serum, plasma, and peripheral blood leukocyte samples of 47 renal transplant donors, 38 recipients with anemia (Group 1), and 25 without anemia (Group 2) after renal transplantation were evaluated for the presence of anti-B19 specific antibodies (ELISA) and B19 DNA (nPCR). Active persistent B19 infection after renal transplantation was detected in 12 of the 38 in the Group 1 (10 had reactivation and 2 primary infection), and none of the recipients in the Group 2 had it. Of the 12 recipients in the Group 1, 10 were seropositive and 2 seronegative before renal transplantation; 10 received the transplants from the seropositive and 2 from seronegative donors. rHuEPO therapy-resistant severe anemia was detected only in the recipients with active B19 infection after renal transplantation in the Group 1 (7/12). The logistic regression analysis revealed a significant relationship between active B19 infection and severe anemia (OR, 0.039; 95% CI, 0.006-0.257; P=0.001). Active B19 infection was documented only in the anemic recipients and could be associated with the development of severe anemia after renal transplantation. This allows us to recommend concurrent screening for viral DNA in plasma and detection of anti-B19 IgM class antibodies. To find the association between B19 infection and the development of anemia, further investigations are necessary.

Highlights

  • Human parvovirus B19 (B19) was first discovered by Cossart et al in the sera of healthy blood donors [1]

  • The logistic regression analysis revealed a significant relationship between active B19 infection and severe anemia (OR, 0.039; 95% CI, 0.006–0.257; P=0.001)

  • The aim of our study was to investigate the frequency of B19 infection in renal transplant donors and patients before and after renal transplantation (RT) and to determine the significance of active viral infection in the development of anemia

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Summary

Introduction

Human parvovirus B19 (B19) was first discovered by Cossart et al in the sera of healthy blood donors [1]. The virus is ubiquitous, and the course of infection depends on the host’s hematological status and immunologic response. A cellular receptor for B19 is globoside (blood group P antigen), which is expressed on erythroid progenitor cells (the site of virus replication), megakaryocytes, tissue cells of the heart, liver, lung, kidney, endothelium, aortic and gastrointestinal smooth muscle, and synovium [2, 3]. The distribution of P antigen across tissues may explain the clinical manifestation of viral infection. The VP proteins contain the domains to which virus-neutralizing antibodies are directed [5]. The appearance of antibodies to B19 is associated with the clearance of the virus from bloodstream; the high frequency of persistence of B19 DNA in the tissues of healthy persons

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