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      Immunity to Polyomavirus BK Infection: Immune Monitoring to Regulate the Balance between Risk of BKV Nephropathy and Induction of Alloimmunity

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          Abstract

          Polyomavirus BK-associated nephropathy (PyVAN) is the main infectious cause of allograft damage after kidney transplantation. A number of studies revealed an association between the presence of BKV-specific cellular immunity and BK viral clearance, with patients failing to recover specific T cells progressing to PyVAN. Evolution to allograft dysfunction can be prevented by restoration of BKV-specific immunity through a stepwise reduction of maintenance immunosuppressive drugs. Prospective monitoring of BK viral load and specific immunity, together with B-cell alloimmune surveillance, may allow a targeted modification/reduction of immunosuppression, with the aim of obtaining viral clearance while preventing graft injury due to deposition of de novo donor-specific HLA antibodies and late/chronic antibody-mediated allograft injury. Innovative, immune-based therapies may further contribute to BKV infection prevention and control.

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          Maintenance of serological memory by polyclonal activation of human memory B cells.

          Nadia Bernasconi, Elisabetta Traggiai, Antonio Lanzavecchia (2002)
          Production of antibodies can last for a lifetime, through mechanisms that remain poorly understood. Here, we show that human memory B lymphocytes proliferate and differentiate into plasma cells in response to polyclonal stimuli, such as bystander T cell help and CpG DNA. Furthermore, plasma cells secreting antibodies to recall antigens are produced in vivo at levels proportional to the frequency of specific memory B cells, even several years after antigenic stimulation. Although antigen boosting leads to a transient increase in specific antibody levels, ongoing polyclonal activation of memory B cells offers a means to maintain serological memory for a human lifetime.
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            BK polyomavirus in solid organ transplantation.

            P Randhawa, Hans H. Hirsch, (2013)
            The human BK polyomavirus (BKV) is the major cause of polyomavirus-associated nephropathy (PyVAN) putting 1-15% of kidney transplant patients at risk of premature allograft failure, but is less common in other solid organ transplants. Because effective antiviral therapies are lacking, screening kidney transplant patients for BKV replication in urine and blood has become the key recommendation to guide the reduction of immunosuppression in patients with BKV viremia. This intervention allows for expanding BKV-specific cellular immune responses, curtailing of BKV replication in the graft, and clearance of BKV viremia in 70-90% patients. Postintervention rejection episodes occur in 8-12%, most of which are corticosteroid responsive. Late diagnosis is faced with irreversible functional decline, poor treatment response, and graft loss. Adjunct therapies such as cidofovir, leflunomide and intravenous immunoglobulins have been used, but the benefit is not documented in trials. Retransplantation after PyVAN is largely successful, but requires close monitoring for recurrent BKV viremia. © Copyright 2013 The American Society of Transplantation and the American Society of Transplant Surgeons.
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              Incidence of BK with tacrolimus versus cyclosporine and impact of preemptive immunosuppression reduction.

              Daniel Bohl, Karen L. Hardinger, Monique Gaudreault-Keener … (2005)
              Our purposes were to determine the incidence of BK viruria, viremia or nephropathy with tacrolimus (FK506) versus cyclosporine (CyA) and whether intensive monitoring and discontinuation of mycophenolate (MMF) or azathioprine (AZA), upon detection of BK viremia, could prevent BK nephropathy. We randomized 200 adult renal transplant recipients to FK506 (n = 134) or CyA (n = 66). Urine and blood were collected weekly for 16 weeks and at months 5, 6, 9 and 12 and analyzed for BK by polymerase chain reaction (PCR). By 1 year, 70 patients (35%) developed viruria and 23 (11.5%) viremia; neither were affected independently by FK506, CyA, MMF or AZA. Viruria was highest with FK506-MMF (46%) and lowest with CyA-MMF (13%), p = 0.005. Viruria >/= 9.5 log(10) copies/mL was associated with a 3-fold increased risk of viremia and a 13-fold increased risk of sustained viremia. After reduction of immunosuppression, viremia resolved in 95%, without increased acute rejection, allograft dysfunction or graft loss. No BK nephropathy was observed. Choice of calcineurin inhibitor or adjuvant immunosuppression, independently, did not affect BK viruria or viremia. Viruria was highest with FK506-MMF and lowest with CyA-MMF. Monitoring and preemptive withdrawal of immunosuppression were associated with resolution of viremia and absence of BK nephropathy without acute rejection or graft loss.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Clin Dev Immunol
                Journal ID (iso-abbrev): Clin. Dev. Immunol
                Journal ID (publisher-id): CDI
                Title: Clinical and Developmental Immunology
                Publisher: Hindawi Publishing Corporation
                ISSN (Print): 1740-2522
                ISSN (Electronic): 1740-2530
                Publication date (Print): 2013
                Publication date (Electronic): 13 August 2013
                Volume: 2013
                Electronic Location Identifier: 256923
                Affiliations
                1Pediatric Hematology/Oncology, Fondazione IRCCS Policlinico San Matteo, 27100 Pavia, Italy
                2Fondazione Malattie Renali del Bambino, Istituto G. Gaslini, 16147 Genoa, Italy
                3Section of Hematology, Department of Medical and Surgical Sciences, University of Modena and Reggio Emilia, 41124 Modena, Italy
                4Pediatric Nephrology, Istituto G. Gaslini, 16147 Genoa, Italy
                Author notes

                Academic Editor: Aron Chakera

                Author information
                http://orcid.org/0000-0001-5964-0553
                Article
                DOI: 10.1155/2013/256923
                PMC ID: 3755406
                PubMed ID: 24000288
                SO-VID: 252f5c5b-73aa-4080-bb5f-1bd348e11e0a
                Copyright © Copyright © 2013 Patrizia Comoli et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 23 February 2013
                Date revision received : 9 July 2013
                Date accepted : 17 July 2013
                Categories
                Subject: Review Article

                ScienceOpen disciplines: Immunology
                Data availability:
                ScienceOpen disciplines: Immunology

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