AbstractPDF
Abstract
Polyomavirus BK (BKV) is ubiquitously present amongst
the general population establishing a latent, seemingly
asymptomatic infection in immunocompetent individuals.
In transplant recipients, however, BKV reactivation is
common and can lead to distinctive pathological entities
in different patient groups: in renal transplant (RT)
recipients, it is associated with nephropathy (BKVN)
and ureteral stenosis, and in haematopoietic stem cell
transplant (HSCT) recipients with haemorrhagic cystitis
(HC). Furthermore, BKV employs several potentially
oncogenic mechanisms to promote its replication in cells
and has been inconsistently linked to the development
of malignancies. BKVN is currently a major cause of
allograft failure in RT recipients. HC causes prolonged
hospital stay and increased mortality in HSCT recipients.
Despite its discovery more than 40 years ago, few advances have been made with regard to therapeutic strategies. Current therapies aim to restore the impaired immune response, e.g. by lowering immunosuppressive agents in RT recipients. However, this is a double-edged sword since it also increases the chance of rejection. Therefore, more specific and effective treatment strategies are urgently needed. Here, we will review the current knowledge on the structure and lifecycle of BKV, characteristics of the
BKV-specific immune response, its clinical manifestations
and the strengths and limitations of available treatments Polyomavirus BK (BKV) is ubiquitously present amongst
the general population establishing a latent, seemingly
asymptomatic infection in immunocompetent individuals.
In transplant recipients, however, BKV reactivation is
common and can lead to distinctive pathological entities
in different patient groups: in renal transplant (RT)
recipients, it is associated with nephropathy (BKVN)
and ureteral stenosis, and in haematopoietic stem cell
transplant (HSCT) recipients with haemorrhagic cystitis
(HC). Furthermore, BKV employs several potentially
oncogenic mechanisms to promote its replication in cells
and has been inconsistently linked to the development
of malignancies. BKVN is currently a major cause of
allograft failure in RT recipients. HC causes prolonged
hospital stay and increased mortality in HSCT recipients.
Despite its discovery more than 40 years ago, few advances have been made with regard to therapeutic strategies. Current therapies aim to restore the impaired immune response, e.g. by lowering immunosuppressive agents in RT recipients. However, this is a double-edged sword since it also increases the chance of rejection. Therefore, more specific and effective treatment strategies are urgently needed. Here, we will review the current knowledge on the structure and lifecycle of BKV, characteristics of the
BKV-specific immune response, its clinical manifestations
and the strengths and limitations of available treatments methods.
