Polyomavirus - an emergent pathogen in transplant recipients Poliomavírus - um patógeno emergente para receptores de transplantes (original) (raw)
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Polyomavirus disease in renal transplantation
Hum Pathol, 2005
Up to 10% of renal transplant recipients can develop polyomavirus nephropathy (PVN) in the allograft, leading to premature graft failure. Recent studies have shown that early diagnosis of PVN before there is irreversible damage to the kidney can result in marked improvement of outcome with resolution of the infection in a large proportion of patients. Early histopathologic diagnosis is complicated by the subtle beginning of the infection and its multifocal nature. This review presents a comprehensive set of guidelines for the effective clinical use of urine cytology and quantitation of viruria and viremia in conjunction with the renal biopsy findings. The morphological features of PVN are presented with specific emphasis on the patterns of PVN that are based on the histological progression of the disease and that correlate with clinical outcome. Also discussed in the context of their clinical significance are the main virological and epidemiological aspects of the BK, JC, and SV40 polyomavirus infections.
Clinical …, 2008
The prevalence of BK polyomavirus infection in outpatient kidney transplant recipients followed in a single center Concurrent with new and more potent immunosuppressive regimens, BK polyomavirus (BKV) infection has recently emerged as an important cause of renal transplant graft loss, an entity called BK nephropathy (1,2). However, risk factors, incidence, prevalence, natural history, and optimal diagnostic and therapeutic strategies have not yet been fully elucidated (3-5). The polyomaviruses, members of the papovavirus family, are small non-enveloped polyhelical double stranded DNA viruses (6). BKV is endemic among humans, but appears to cause disease only when the host is significantly immunosuppressed (7). Most primary infections are asymptomatic, and up to 80% of children develop anti-BKV antibodies by age 6-8 (8). After primary infection, the virus remains latent in the host urogenital epithelium (9). Viral reactivation may occur, associated with diseases or therapy causing immunosuppression like renal transplantation (10,11). During reactivation, viruria occurs with exfoliation of urinary epithelial cells containing intranuclear BKV viral particles, known as ''decoy cells'' (12). These are not specific for BKV infection, but
Liver Transplantation, 2006
JC virus (JCV), BK virus (BKV) and simian virus 40 (SV40) are deoxyribonucleic acid (DNA) viruses, members of the family Polyomaviridae. These viruses establish persistent infections, and reactivate from latency in their host under immunosuppression. During the last few years there has been recognition of the morbidity related to polyomaviruses, particularly BKV in kidney transplant recipients. More importantly, recent studies indicate the potential implication of JCV, BKV, and SV40 in renal dysfunction among nonrenal organ transplant patients. Polyomaviruses are tumor-inducing viruses and animal models have provided evidence of the oncogenicity of these pathogens. Although data are not conclusive, molecular studies suggest an association of BKV and SV40 with malignancies among solid organ transplant patients. As new and potent immunosuppressive agents are introduced into clinical practice, it is believed that the incidence of polyomavirus-related diseases in organ transplantation might increase. This review evaluates the biologic and epidemiologic features of these 3 viruses, the data regarding their infections in nonkidney organ transplant patients and describes future directions in the management and research of these opportunistic pathogens.
Human pathology, 2005
Up to 10% of renal transplant recipients can develop polyomavirus nephropathy (PVN) in the allograft, leading to premature graft failure. Recent studies have shown that early diagnosis of PVN before there is irreversible damage to the kidney can result in marked improvement of outcome with resolution of the infection in a large proportion of patients. Early histopathologic diagnosis is complicated by the subtle beginning of the infection and its multifocal nature. This review presents a comprehensive set of guidelines for the effective clinical use of urine cytology and quantitation of viruria and viremia in conjunction with the renal biopsy findings. The morphological features of PVN are presented with specific emphasis on the patterns of PVN that are based on the histological progression of the disease and that correlate with clinical outcome. Also discussed in the context of their clinical significance are the main virological and epidemiological aspects of the BK, JC, and SV40 p...
JRMS, 2011
BACKGROUND: Post-transplant infection with polyoma viruses (BK and JC viruses) is an important cause of graft loss and nephropathy. The objective of this study was to compare the frequency of BK and JC viruria in renal transplant recipients with and without graft dysfunction. METHODS: In a case-control study, we selected 60 kidney transplant patients with and without graft dysfunction in the first two years after transplantation. Each group consisted of 30 patients evaluated for basic demographic and laboratory characteristics. First morning urine samples were sent for BK and JC virus detection with QIAamp DNA Mini Kit and real-time polymerase PCR. Chi-square test with Yates' correction, Student t-test and Mann-Whitney U test were used as indicated. P value of less than 0.05 was regarded as statistically significant. RESULTS: Both groups were similar in age, gender, and time after transplant and pretransplant dialysis. In both groups, seven patients (23.3%) were JC virus positive whereas in case group 14 patients (46.7%) and in control group 9 patients (30%) were BK virus positive. There were no statistical significant difference between case and control groups for both JC and BK virus infection rate. CONCLUSIONS: We concluded that JC and BK virus infection is very prevalent in the first 2 years after transplant and might be monitored appropriately.
Rapid Dynamics of Polyomavirus Type BK in Renal Transplant Recipients
The Journal of Infectious Diseases, 2006
Background. Polyomavirus type BK-associated nephropathy (PVAN) is an emerging cause of early renal transplant failure. No specific antiviral treatment has been established. Current interventions rely on improving immune functions by reducing immunosuppression. In patients with PVAN, a high BK virus (BKV) load is detectable in plasma. However, the relationship between BKV replication and disease is not well understood.
BK polyomavirus infection after renal transplantation: Surveillance in a resource-challenged setting
Transplant infectious disease : an official journal of the Transplantation Society, 2017
A paucity of data is available about BK polyomavirus (BKPyV) infection after renal transplantation (RTX) in resource-limited countries with a predominantly living-donor, ABO-compatible RTX program. We aimed to assess BKPyV infection in such patients in a public hospital in India. We prospectively evaluated plasma BKPyV replication in 62 patients at 1, 3, 6, 9, 12 months after RTX. Sustained significant BK viremia (SSBKV) was defined as significant viremia (≥10 000 copies/mL) detected ≥2 times and BKPyV-associated nephropathy (BKVAN) as histologic changes of BKVAN with BK viremia with/without graft dysfunction. All patients underwent RTX without requiring desensitization. Incidence of BK viremia was: 17.7%, 41.9%, 16.1%, 25.8%, and 17.7% at 1, 3, 6, 9, and 12 months respectively. 64.5% patients had BKPyV viremia during the study, 32.2% had significant viremia, all except one detected in the first 6 months. Nine (14.5%) patients had SSBKV. At the end of 1 year, mean serum creatinine w...
Polyomavirus BK and JC infections in well matched Finnish kidney transplant recipients
Transplant International, 2009
Since 2003, only one case of polyomavirus-associated nephropathy (PVAN) has occurred in our clinic despite screening protocols. In contrast to BK virus, the role of JC virus in PVAN is unclear. We studied the incidence and impact of polyomavirus BK and JC viruria and PVAN in well-matched Finnish kidney transplant recipients. All Helsinki University Hospital kidney transplant recipients between 2004 and 2006 were prospectively followed (n = 163). Patients with a 12-month protocol-biopsy taken and polyomavirus urinary secretion screened by PCR were studied (n = 68). Cyclosporine-based triple-drug immunosuppression was usually used. BK or JC viruria was detected in 18 (27%) and 14 (21%) patients after transplantation respectively. Persistent BK or JC viruria was found in 5 (7%) and 9 (13%) patients. No cases of PVAN were diagnosed from protocol biopsies or from biopsies taken for clinical indications. A positive BK or JC viruria or persistent viruria was not associated with reduced renal function at follow-up, histopathologic changes in 12-month protocol biopsies, or acute rejections. The incidence of BK and JC viruria was similar to what has been previously reported, but no cases of polyomavirus-associated nephropathy were seen in our well-matched kidney transplant population.
Iranian Journal of Pathology, 2022
Scan to discover online Background & Objective: Polyomaviruses types BK and JC and Cytomegalovirus (CMV) have been shown to be related to kidney transplantation complications. This study aimed to assess the prevalence of these viruses in patients receiving kidney transplantation. Methods: This cross-sectional study was performed on 40 kidney transplant recipients and 44 donors. Urine samples were used for the extraction of viral DNA. The prevalence of JC and BK viruses and their viral loads were determined by real-time polymerase chain reaction. Results: JC and BK viruses were identified in 31% and 92.3% of all subjects, respectively. The frequency of JC and BK cases was not statistically different between the recipient and donor groups (P>0.05). All patients in the donor group and 96.8% of the recipients were positive for CMV IgG antibody. The mean viral load of BK in donors and recipients was 4.5×10 10 and 3.3×10 11 copies, respectively. The mean viral load of JC was 8.6×10 7 copies in donors and 2.9×10 8 copies in recipients. The distribution of BKV was significantly higher in recipients than donors (P=0.001), while no difference was observed between the two studied groups for JCV. Conclusion: This study showed a relatively high prevalence of BK and JC viruria in both renal transplant donors and recipients. The viral load for BKV, but not JCV, was higher in recipients than in donors.