Simian virus 40 (SV40), a monkey polyomavirus that is believed to have entered the human population through contaminated vaccines, is known to be renotropic in simians. If indeed SV40 is endemic within the human population, the route of transmission is unknown. It was therefore hypothesized that SV40 might be renotropic in humans and be detected more frequently in samples obtained from patients with kidney diseases. This study found that typical polyomavirus cytopathic effects (CPE) were present and SV40 T antigen was detected in CV-1 cells cultured with peripheral blood mononuclear cells (PBMC) or urinary cells obtained from patients with kidney disease and healthy volunteers. DNA sequences homologous to the SV40 viral regulatory genome were detected by PCR in urinary cells from 15 (41%) of 36 patients with focal segmental glomerulosclerosis (FSGS), 2 (10%) of 20 patients with other kidney diseases, and 1 (4%) of 22 healthy volunteers (FSGS compared with other glomerular disease, P < 0.02; FSGS compared with healthy volunteers, P = 0.003). SV40 viral regulatory region genome was detected from PBMC at similar frequencies in patients with FSGS (35%), other glomerular diseases (20%), and healthy volunteers (22%). SV40 genome was detected by PCR in kidney tissues from 17 (56%) of 30 of patients with FSGS and 4 (20%) of 20 patients with minimal change disease and membranous nephropathy (P < 0.01). Considerable genetic heterogeneity of the viral regulatory region was detected, which argues against laboratory contamination. SV40 genome was localized to renal tubular epithelial cell nuclei in renal biopsies of patients with FSGS by in situ hybridization. This study demonstrates for the first time that human kidney can serve as a reservoir for SV40 replication and that SV40 may contribute to the pathogenesis of kidney disease, particularly FSGS.
[Show abstract][Hide abstract] ABSTRACT: Background
Collapsing glomerulopathy may occur in an idiopathic (primary) form and in association with a wide spectrum of infectious and inflammatory conditions and medications. The association of collapsing glomerulopathy with human immunodeficiency virus (HIV)-1 infection is well established; less certain is the association with other viral infections.
We searched PubMed for articles in all languages that addressed glomerulopathies associated with parvovirus B19, cytomegalovirus (CMV), Epstein-Barr virus (EBV), hepatitis C virus (HCV) and simian virus 40 (SV40).
Case reports and small-case series link infection with these common viruses and glomerular injury. The evidence for a pathogenic role is generally stronger for glomerulonephritis than for collapsing glomerulopathy.
The evidence linking collapsing glomerulopathy with CMV is relatively strong but not yet conclusive, while the evidence for a pathogenic role for EBV and parvovirus B19 is weaker.
"Virus activity begins in immunocompromised conditions such as immunosuppressed kidney transplant recipients and HIV positive patients [2, 6, 7]. Although SV40 was isolated from kidney transplant biopsies, its importance has not already been well described [8, 9]. Both BK and JC viruses were identified in 1971, but their significance was limited . "
[Show abstract][Hide abstract] ABSTRACT: Background: BK virus nephropathy (BKVN) is one of the complications of renal transplantation that causes graft loss in renal transplant recipients.
Objective: To determine the incidence of BKVN after renal transplantation in Hasheminejad Hospital, Tehran, Iran.
Methods: In this analytical cross-sectional study, we evaluated 31 consecutive kidney transplant recipients (21 men and 10 women) for BK and JC viral infections and BKVN during one year after transplantation, Urine of patients was tested for the presence of decoy cells and DNA of BK and JC virus by PCR. The serum load of BK and JC virus was assessed in patients 3, 6, 9, and 12 months after transplantation. Renal biopsy was performed in presence of allograft dysfunction or viral load >107 copies/mL.
Results: The prevalences of decoy cells and BK and JC viral DNA in urine of patients were 16%, 29%, and 23%, respectively. BK or JC virus was found in 45% of the urine samples. During one year follow-up, no cases of BKVN was observed.
Conclusion: Despite a high rate of BK viral infection, no one with BKVN was observed in our kidney transplant recipients. Therefore, screening of all transplant recipients for BKVN is not recommended.
International Journal of Organ Transplantation Medicine 08/2012; 3(3):115-8.
"More recently, using DNA molecular amplification methods, the presence of SV40 sequences has been reported in samples obtained from a variety of human tumors including choroid plexus tumors (Bergsagel et al., 1992; Lednicky et al., 1995a), ependymomas (Bergsagel et al., 1992; Lednicky et al., 1995a), mesotheliomas (Barbanti-Brodano et al., 1998; Carbone et al., 1994; Pepper et al., 1996; Rizzo et al., 1998, 1999a; Vilchez and Butel, 2003a), osteosarcomas (Carbone et al., 1996; Heinsohn et al., 2000; Lednicky et al., 1997; Rizzo et al., 1998), glioblastomas (Kouhata et al., 2001), and non-Hodgkin's lymphomas (Butel et al., 2003; Vilchez and Butel, 2003b). In addition, SV40 has been reported to be present in patients with renal allografts and focal segmental glomerulosclerosis (Li et al., 2002a,b). SV40 DNA sequences have also been reported to be present in the peripheral blood mononuclear cells of normal donors (Martini et al., 2002) and recently in the urine (Vanchiere et al., 2005b) and stools (Vanchiere et al., 2005a) of children. "
[Show abstract][Hide abstract] ABSTRACT: From stocks of adenovirus and poliovirus prepared in primary rhesus macaque kidney cells and dating from 1956 to 1961, the time when SV40 contaminated some poliovirus vaccine lots, we have recovered ten isolates of SV40. Of these ten isolates, based on the C-terminal region of T antigen, five novel strains of SV40 have been identified. Additionally, three pairs of isolates were found to be the same strain: one pair was strain 777, one pair was strain 776 archetype, and the third pair represented a novel strain. All strains had identical protein sequences for VP2 and VP3. There were two variants of agnoprotein and the small t antigen and three variants of VP1. These results, and those of others, suggest that a limited number of SV40 strains might exist in rhesus macaques in the United States, and thus determining the origin of the SV40 sequences detected in human tumors might be difficult.
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