Abstract

This study evaluated the relative occurrences of BK virus (BKV) and JC virus (JCV) infections in patients with chronic kidney disease (CKD). Urine samples were analysed from CKD patients and from 99 patients without CKD as a control. A total of 100 urine samples were analysed from the experimental (CKD patients) group and 99 from the control group. Following DNA extraction, polymerase chain reaction (PCR) was used to amplify a 173 bp region of the gene encoding the T antigen of the BKV and JCV. JCV and BKV infections were differentiated based on the enzymatic digestion of the amplified products using BamHI endonuclease. The results indicated that none of the patients in either group was infected with the BKV, whereas 11.1% (11/99) of the control group subjects and 4% (4/100) of the kidney patients were infected with the JCV. High levels of urea in the excreted urine, low urinary cellularity, reduced bladder washout and a delay in analysing the samples may have contributed to the low prevalence of infection. The results indicate that there is a need to increase the sensitivity of assays used to detect viruses in patients with CDK, especially given that polyomavirus infections, especially BKV, can lead to a loss of kidney function following transplantation.

Highlights

  • Two human polyomaviruses (BK and JC) were discovered more than 40 years ago (Gardner et al 1971, Padgett et al 1971)

  • This study aimed to evaluate the relative prevalence of JC virus (JCV) and BK virus (BKV) infections in kidney transplant candidates with chronic renal disease from the Brazilian state of Acre (AC) and the possible association between clinical or laboratory factors of disease and socio-demographic variables

  • Prevalence of polyomaviruses - The JCV was identified in 11.1% (11/99) of the subjects in the control group and 4% (4/100) of those in the chronic kidney disease (CKD) patient group (Table IV)

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Summary

Introduction

Two human polyomaviruses (BK and JC) were discovered more than 40 years ago (Gardner et al 1971, Padgett et al 1971). Primary infection with BKV possibly occurs through the respiratory tract during early childhood, with the virus remaining dormant in the urinary tract and other organs (Goudsmit et al 1982) This primary infection is usually asymptomatic, but it may induce a fever and nonspecific respiratory symptoms (Reploeg et al 2001). Reactivation of the BKV may occur spontaneously in immunocompetent subjects and is relatively frequent in individuals with impaired cellular immunity, such as pregnant women, cancer patients receiving chemotherapy, AIDS patients and transplant recipients In these patients, the virus can cause haemorrhagic cystitis, nephritis, urethral stenosis and a loss of function of the transplanted kidney (Coleman et al 1978, Gardner et al 1984, Chan et al 1994, Weiskittel 2002). The presence of BKV has been associated with rejection of the transplanted kidney, whereas JCV has been associated with nonspecific symptoms in the transplanted kidney, lungs and pancreas (Weiskittel 2002)

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