BK and JC polyomaviruses (BKV and JCV) are widespread in humans and are thought to persist and reactivate under immune alterations. In addition to the kidney, lymphoid cells have been proposed as a site of latency. However, while this was shown to occur in immunocompromised patients, discordant data were published for healthy humans. To help to solve this issue, an extensive study (231 healthy subjects) was carried out on peripheral blood mononuclear cells (PBMC) from blood donors of two towns and from operators of a blood transfusion centre. To discriminate between past and recent infection, nested PCRs for BKV and JCV non-coding control region (NCCR) and VP1 DNA sequences were carried out. Twenty-two per cent of subjects had BKV NCCR, but only 7% also had BKV VP1, as detected by PCR assays of similar sensitivities; the latter positivity was found to decrease with age. In both towns, the BKV WW archetypal DDP strain, subtype I, was found. Only 0.9% of subjects contained JCV DNA, for both NCCR and VP1. Blood operators presented a statistically significant increased prevalence of BKV NCCR (3. 0-fold) and BKV VP1 (9.4-fold) sequences with respect to blood donors of comparable ages, suggesting the possibility of occupational risk of BKV (re)infection or reactivation. Since the possibility of amplifying BKV VP1 sequences from PBMC of healthy humans is lost with age, this suggests that PBMC are not a site of polyomavirus persistence in healthy individuals and that detection of BKV VP1 DNA in PBMC is probably indicative of recent infection or reactivation.
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http://dx.doi.org/10.1099/0022-1317-81-8-1967 | DOI Listing |
BK polyomavirus (BKV) causes polyomavirus-associated nephropathy (PyVAN) and polyomavirus-associated hemorrhagic cystitis (PyVHC) following kidney transplantation and allogeneic hematopoietic stem cell transplantation (HST). BKV strains fall into four distinct genotypes (BKV-I, -II, -III, and -IV) with more than 80% of individuals are seropositive against BKV-I genotype, while the seroprevalence of the other four genotypes is lower. PyVAN and PyVHC occurs in immunosuppressed (e.
View Article and Find Full Text PDFEBioMedicine
December 2024
University College London Institute of Immunity and Transplantation, Royal Free Hospital, London, UK. Electronic address:
Background: BK polyomavirus (BKV) DNAaemia occurs in 10% of recipients of kidney transplants, contributing to premature allograft failure. Evidence suggests disease is donor derived. Hypothetically, recipient infection with a different BKV serotype increases risk due to poorer immunological control.
View Article and Find Full Text PDFAm J Transplant
November 2024
Novartis Institutes for BioMedical Research, Translational Medicine, East Hanover, New Jersey, USA.
Reactivation of BK polyomavirus (BKPyV) can cause significant kidney and bladder disease in immunocompromised patients. There are currently no effective, BKPyV-specific therapies. MAU868 is a novel, human immunoglobulin (Ig) G1 monoclonal antibody that binds the major capsid protein, VP1, of BKPyV with picomolar affinity, neutralizes infection by the 4 major BKPyV genotypes (EC ranging from 0.
View Article and Find Full Text PDFInt J Mol Sci
December 2023
Department of Internal Medicine III, Division of Nephrology and Dialysis, Medical University of Vienna, 1090 Vienna, Austria.
Polyomaviruses are widespread, with BK viruses being most common in humans who require immunosuppression due to allotransplantation. Infection with BK polyomavirus (BKV) may manifest as BK virus-associated nephropathy and hemorrhagic cystitis. Established diagnostic methods include the detection of polyomavirus in urine and blood by PCR and in tissue biopsies via immunohistochemistry.
View Article and Find Full Text PDFFront Immunol
November 2023
Resesarch and Development Institute for In Vitro Diagnostic Medical Devices, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea.
Introduction: Polyomavirus (BKV) infection can lead to major complications and damage to the graft in kidney transplant recipients (KTRs). We investigated whether pretransplant BK serostatus and BK-specific cell-mediated immunity (CMI) predicts post-transplant BK infection.
Methods: A total of 93 donor-recipient pairs who underwent kidney transplantation (KT) and 44 healthy controls were examined.
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