Prevalence of infection by JC and BK polyomaviruses in kidney transplant recipients and patients with chronic renal disease

Abstract

The present study investigated the prevalence of infection by JC and BK polyomaviruses (JCV and BKV) in patients with chronic renal disease (CRD), kidney transplant recipients, and a control group of asymptomatic subjects. We tested a total of 295 urine samples. After DNA extraction, polymerase chain reaction assay was used to amplify a fragment of 173 bp of the polyomavirus T antigen, followed by analysis using the BamHI restriction endonuclease. Infection by polyomavirus was detected in 17.6% (52/295 subjects) of the subjects. Whereas 30.5% (18/59) of transplant recipients were infected, the frequency was only 22.4% (30/134) in the control subjects, and 3.9% (4/102) in the CRD group (all JCV). The vast majority of infections (88.9%; 16/18) in transplant recipients were of the BKV type, whereas this type was absent in CRD patients, and made up only 10.0% (3/30) of infections in the control group. The risk of BKV infection was 72 times greater in renal transplant patients than in asymptomatic subjects. The low frequency of infection found in CRD patients may have been related to elevated levels of urea excreted in the urine, together with reduced urine volume and cell content. These factors may combine to reduce viral load or inhibit amplification. The results of the study indicate a need for the routine screening for polyomavirus in pre- and post-transplant patients, as well as organ donors, considering that BKV infection has been associated with graft rejection in kidney transplants.

JC polyomavirus infection in candidates for kidney transplantation living in the Brazilian Amazon Region

“…The polyomavirus infection rates recorded in this study were considerably lower than those reported in other Brazilian populations (Cayres- Vallinoto 2008, Pires et al 2011). Cayres-Vallinoto (2008 reported a JCV infection rate of 33% in the city of Belém, state of Pará, whereas Pires et al (2011) reported prevalence of 3.9% in patients diagnosed with CKD and 22.4% in asymptomatic subjects.…”

“…Molecular analysis -The presence of JCV and/or BKV was evaluated by amplifying a 173 bp fragment of the gene encoding the T antigen of both viruses, which was amplified by polymerase chain reaction (PCR) as described by Pires et al (2011). DNA samples from previously confirmed JCV and BKV infected subjects, stored at -20ºC, were used as positive controls in all PCR assays.…”

“…The products of this digestion were visualised using 3% agarose gel electrophoresis as previously described (Pires et al 2011).…”

“…At the UFPA Virus Laboratory, the samples were centrifuged at 3,640 g for 15 min until the urine residue was completely separated. The sediment was then washed three times with a sterile saline solution (0.9%) and the cell pellet was frozen at -20ºC until the DNA could be extracted, as described by Pires et al (2011).…”

“…This polyomavirus causes tubulointerstitial nephritis in the kidney tissue, which is known as polyomavirus-associated nephropathy (Hirsch et al 2006). The detection of polyomaviruses in kidney transplant candidates (patients with chronic renal disease) should be a standard component of pre-transplant research, especially given the potential role these viruses play in graft rejection (Pires et al 2011). The differential diagnosis of these viruses is also essential, given that they are histologically similar, but require distinct courses of treatment (Elli et al 2002).…”