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JC virus DNA in the peripheral blood of renal transplant patients: A 1‐year prospective follow‐up in France
Author(s) -
Mengelle C.,
Kamar N.,
Mansuy JM.,
SandresSauné K.,
LegrandAbravanel F.,
Miédougé M.,
Rostaing L.,
Izopet J.
Publication year - 2011
Publication title -
journal of medical virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.782
H-Index - 121
eISSN - 1096-9071
pISSN - 0146-6615
DOI - 10.1002/jmv.21951
Subject(s) - jc virus , progressive multifocal leukoencephalopathy , bk virus , medicine , viral load , immunosuppression , rituximab , transplantation , immunology , virus , virology , nephropathy , tacrolimus , gastroenterology , kidney transplantation , antibody , diabetes mellitus , endocrinology
There is little information on JC virus (JCV) infection in renal transplant patients. A long‐term prospective follow‐up study was conducted to assess the incidence of JCV DNA in the blood of 103 adult renal transplant patients enrolled prospectively between 1 January and 31 December 2006. Patients were monitored until April 2008. JCV DNA was quantified by a real‐time polymerase chain reaction in whole blood samples collected regularly for at least 1 year post‐transplant. JCV was detected in seven patients (6.8%) (31/1,487 whole blood samples) at a median time of 139 days post‐transplant. The median JC virus load of the first positive DNA blood sample was 3.4 log 10 copies/ml (1.9–5.7 log 10 copies/ml). Induction therapy were either anti‐CD25 monoclonal antibodies (n = 5) or antithymocyte globulins (n = 2). Post‐transplant immunosuppressive treatment included steroids with tacrolimus/mycophenolate mofetil (MMF) (n = 2), or ciclosporin/MMF (n = 1), or belatacept/MMF (n = 4). Two patients were also treated with rituximab. All seven patients infected with JCV had other viral infections(s): BK virus (3), Epstein–Barr virus (2), Cytomegalovirus (1) or both BK virus and Epstein–Barr virus (1). Three patients had BKV‐associated nephropathy and decoy cells shedding. JCV infection was not associated with acute rejection episodes or nephropathy, regardless of the virus load. No patient developed progressive multifocal leukoencephalopathy during follow‐up. Thus the incidence of JCV infection in renal transplant patients was low and not associated with any specific clinical manifestations. JCV replication must still be diagnosed and differentiated from BK virus infection because of its non‐aggressive course. J. Med. Virol. 83:132–136, 2011. © 2010 Wiley‐Liss, Inc.