The detection of BKPyV genotypes II and IV after renal transplantation as a simple tool for risk assessment for PyVAN and transplant outcome already at early stages of BKPyV reactivation

Le virus BK (BKV) appartient a la famille des Polyomaviridae. Il est largement repandu dans la population generale adulte. La primo-infection, generalement asymptomatique, se deroule pendant l’enfance. Puis, le virus persiste sous forme latente dans l’organisme, principalement dans les cellules epitheliales du rein et du tractus urinaire. L’immunodepression cellulaire favorise la reactivation du BKV. Apres transplantation renale, l’infection active a BKV peut etre a l’origine de nephropathies tubulo-interstitielles allant jusqu’a la perte du greffon. Chez les patients recevant une greffe de cellules souches hematopoietiques, elle est generalement associee a la survenue de cystites hemorragiques (CH) tardives. La physiopathologie de ces CH semble correspondre a une interaction entre les dommages cellulaires causes par le conditionnement pre-greffe, l’infection active a BKV et la reaction allo-immune des lymphocytes du donneur diriges contre les cellules de l’uroepithelium du receveur. Le diagnostic virologique des CH repose sur la quantification du genome du BKV par PCR dans les urines et le sang. La prise en charge de cette pathologie consiste avant tout en un traitement symptomatique, aucun traitement antiviral specifique n’ayant clairement demontre son efficacite.

Infections à virus BK après allogreffe de cellules souches hématopoïétiques

The relation of NCCR variations and host transcription factors gene regulation in BK polyomavirus infected kidney transplant patients.

The human BK Polyomavirus (BKPyV) is a DNA virus that is prevalent in 80 % of the population. Infection with this virus may begin in childhood, followed by asymptomatic persistence in the urinary tract. However, in immunocompromised individuals, especially kidney transplant recipients (KTRs), heightened replication of BKPyV can lead to severe complications. The genome of this virus is divided into three parts; the early and late region, and the non-coding control region (NCCR). Mutations in the NCCR can change the archetype strain to the rearranged strain, and NCCR rearrangements play a significant in virus pathogenesis. Interestingly, diverse types of NCCR block rearrangement result in significant differences in conversion potential and host cell viability in the infected cells. A correlation has been detected between increased viral replication potential and pathogenesis in BKPyV-infected KTRs with specific NCCR rearrangements. The objective of this review study was to examine the disease-causing and clinical consequences of variations in the NCCR in BKPyV-infected KTRs such as virus-associated nephropathy (BKPyVAN). 

Impact of BK Polyomavirus NCCR variations in post kidney transplant outcomes.

BK polyomavirus (BKPyV) is a human pathogen that infects the majority of the population, worldwide, establishing a lifelong infection. Immunocompromised patients following renal transplantation, are likely to suffer from severe clinical complications, including polyomavirus-associated nephropathy (PVAN), which can ultimately lead to kidney graft failure. Currently, there are no direct acting anti-viral compounds targeting BKPyV and the number of renal transplants is increasing significantly. Therefore, there is an urgent need to understand the viral life cycle in order to identify potential targets that can be exploited for therapeutic development. 
Ion channels play a critical role in kidney physiology by controlling several processes, implicating them as candidate proteins required for BKPyV infection. A pharmacological analysis was performed in which human primary renal epithelial cells were treated with a range of pharmacological modulators of host ion channels and the effect on BKPyV production assayed using a fluorescence-based technique. From this approach, it was identified that the clinically available drug, Glibenclamide is a potent inhibitor of BKPyV infection. Biochemical analysis and molecular-based techniques revealed that the cystic fibrosis transmembrane conductance regulator (CFTR) was the target of Glibenclamide and time-of-addition experiments indicated that CFTR might be required during the entry and trafficking of BKPyV through the cytoplasm. These studies provide the first reported requirement for host ion channels in the BKPyV life cycle.
Studies on other related polyomaviruses, including JCPyV, SV40 and Merkel cell polyomavirus determined a cell type-dependent requirement of CFTR in the viruses’ life cycle, highlighting the importance of understanding the role of host ion channels in polyomaviruses’ life cycle. Ion channels are an emerging target for many medical conditions and such compounds that target these may represent a novel strategy for developing therapeutics to treat PVAN and/or other polyomavirus-associated clinical complications.

Role of cellular ion channels in the BK polyomavirus life cycle

The BK polyomavirus (BKPyV) is one of the main human polyomaviruses. After primary infection, it establishes a persistent infection, and acts as an opportunistic pathogen, innocuous in immunocompetent hosts, but causing potentially serious pathology in the context of immunosuppression, in particular in kidney and hematopoietic stem cell graft recipients. Much progress has been made in recent years in the description of virus-cell interactions, but many aspects of viral physiopathology remain mysterious, principally due to the asymptomatic nature of infection in immunocompetent individuals and the lack of an animal model. The characteristics of the antiviral immune response are beginning to become more clearly understood, particularly in kidney transplant patients. Work in these areas is important in order to identify patients at high risk of developing a severe infection. Indeed, in the absence of an effective antiviral therapy few therapeutic options are available, and patient management remains based on modulation of immunosuppressive therapy.

BK polyomavirus: virus-cell interactions, host immune response, and viral pathogenesis

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BK polyomavirus: virus-cell interactions, host immune response, and viral pathogenesis