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.
Highlights
The morbidity and mortality of viral infections are significantly increasing in transplant patients
Polyomavirus BK (BKV), first isolated in the 1970s, is a double-stranded DNA virus with a genome structure consisting of the early nonstructural genes encoding large T and small t antigens, the late genes encoding the capsid proteins (VP1, VP2, and VP3) and the agnoprotein and a noncoding control region (NCCR) harboring viral promoters and the origin of replication [2]
BKV-related nephropathy (PyVAN) was initially reported to cause graft loss in 10% to >80% of cases [5,6,7,8], but implementation of BKV monitoring strategies after transplantation and prompt/preemptive therapeutic intervention had a positive impact on graft outcome [6, 9, 10]
Summary
The morbidity and mortality of viral infections are significantly increasing in transplant patients. Prevalence and level of BKV replication in urine, occasionally observed in healthy individuals [4], may increase with pregnancy, kidney disease, and immunodeficiency status including hematopoietic stem cell and renal transplantation [2]. In the latter setting, BKV has emerged in the last 15 years as the most challenging infectious cause of renal allograft dysfunction and graft loss [5]. As control of infection depends on the restoration of a protective immune response, characterization of specific viral immunity has facilitated development of recombinant or cellular vaccines [13,14,15]. We will review available evidence on BKV-specific immune responses, suggest an immunological monitoring approach to the management of BKV reactivation and PyVAN, and discuss possible future immune-based therapeutic options
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