VIROLOGICAL ASPECTS: Human polyomaviruses (BK virus and JC virus), together with simian polyomaviruses (SV40 virus) share 75% of genomic homology. Their in vivo and in vitro genomes vary. Molecular analyses have identified several genotypes, some of which appear related to the development of viral diseases. Genomic modifications of the regulation area might provide the BKv with a pathogenic aspect thus enhancing the induction of tubulo-interstitial nephropathies in renal transplant recipients.
Epidemiology: Human polyomaviruses are ubiquitous and exhibit a sero-prevalence of 60 to 80% in adults. Following a primary infection via the respiratory tract in childhood, these viruses are diffused in the blood using the B-lymphocytes during their latent stage in the urogenital tract. The reactivation that occurs after several years is asymptomatic and urinary excretion of BKv is observed in 4 to 6% of immunocompetent patients.
Pathogenic potential: Human polyomaviruses have a cytopathogenic effect on the urothelium and epithelium of renal transplant recipients. Infection by BKv may provoke hemorrhagic cystitis or urethral stenosis. The JCv is the cause of progressive multifocal leuko-encephalitis. The BKv (and less frequently the JCv) is responsible for tubulo-interstitial nephritis possible leading to renal transplant loss. They also have an oncogenic effect and their implication in the origin of tumours is the subject of many studies.