Latent and Persistent Polyomavirus Infection

Histological Patterns of Polyomavirus Nephropathy: Correlation with Graft Outcome and Viral Load

“…Irrespective of the underlying etiopathogenesis, florid inflammatory responses in PVAN are often associated with parenchymal fibrosis (scarring) (9,29). Therefore, as suggested previously it is possible that undiagnosed low-level PVAN may be the etiology of graft sclerosis in some patients (chronic allograft nephropathy) (23).…”

Evolution of the BK polyomavirus: epidemiological, anthropological and clinical implications

“…BKV strains are classified into four subtypes using serological and genotyping methods [4]. Asymptomatic infection with BKV occurs during early childhood, with subsequent life-long persistence in the kidney [5]. Renal BKV infection is usually subclinical [5] and diseases caused by BKV are linked to a decline in immunologic activity [6].…”

“…Asymptomatic infection with BKV occurs during early childhood, with subsequent life-long persistence in the kidney [5]. Renal BKV infection is usually subclinical [5] and diseases caused by BKV are linked to a decline in immunologic activity [6]. For example, BKV may cause graft dysfunction and loss in renal transplant recipients undergoing immunosuppressive therapy; a condition referred to as polyomavirus-associated nephropathy (PVAN) [7].…”

Periodic Assessment of Urine and Serum by Cytology and Molecular Biology as a Diagnostic Tool for BK Virus Nephropathy in Renal Transplant Patients

“…1 After primary exposure, the viruses become latent, and their genomic sequences can be detected only by polymerase chain reaction (PCR) in kidney and urinary tract tissues (JCV and BKV), brain tissue (JCV) and, more rarely, other organs in healthy individuals. [2][3][4][5] Various diseases can be triggered by virus reactivation, the frequency of which changes in patients with different types of immune impairment: JCV is the cause of progressive multifocal leukoencephalopathy (PML), a demyelinating disease of the central nervous system affecting mainly AIDS patients, 6 whereas BKV reactivation in the renal parenchyma causes tubulointerstitial nephropathy (PVN) almost exclusively in renal allograft recipients. 7 Hemorrhagic cystitis and ureteral stenosis have occasionally been associated with JCV and/or BKV in patients undergoing bone marrow and renal transplantation.…”