Objectives: To examine the prevalence of polyomavirus SV40 infections in Kazakhstan, a central Asian country known to have used potentially contaminated SV40 poliovaccines before 1962.
Methods: Cross-sectional study of 307 healthy volunteers from two ethnic groups (Kazakhs and Russians) in Almaty, Kazakhstan, from May through August 1999 using a specific SV40 plaque-reduction neutralization assay.
Results: Of the 307 volunteers enrolled in the study, 154 were Kazakhs and 153 were Russians. The overall prevalence of SV40 antibodies was 4.9%, and there was no significant difference between the ethnic groups (p = 0.7) or between males and females. The median SV40 neutralizing antibody titers in Kazakhs and Russians were 1:40 (range 1:10-1:500) and 1:20 (range 1:10-1:500), respectively. The median ages of SV40-infected Kazakhs and Russians were not different (42 vs. 24 years; p = 0.1), although there was a trend for increased seropositivity among older Kazakhs. There was no difference in SV40 positivity between those whose childhoods were spent in rural or in urban areas (p = 0.4). Importantly, 60% (9/15) of the subjects seropositive for SV40 were born from 1969 to 1980s, when poliovaccines were free from SV40.
Conclusions: This study showed evidence of polyomavirus SV40 infections in Kazakhstan, not only among individuals potentially exposed to contaminated poliovaccines, but in younger people not exposed to such vaccines. As increasing evidence indicates an association of SV40 with selected types of human malignancies, prospective studies are needed to examine the risk of SV40 infection with the development of neoplasias.
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http://dx.doi.org/10.1016/j.jinf.2004.03.001 | DOI Listing |
Ann Diagn Pathol
December 2024
Department of Pathology and Genomic Medicine, Houston Methodist Hospital, Houston, Texas, United States - 77030.
BK Polyomavirus nephropathy (PVN) with definitive diagnosis on biopsy, presents incidentally or with varying degrees of graft dysfunction. Banff working group on PVN has proposed a novel scoring system in renal biopsies, to identify patients with higher risk of graft failure. In this study, we attempted to validate the Banff scoring system at index biopsies and correlate with a novel index score, plasma BK-virus load and graft outcome.
View Article and Find Full Text PDFTumour Virus Res
December 2024
Department of Biological Sciences, University of Pittsburgh, Pittsburgh, PA, 15260, USA. Electronic address:
PLoS Pathog
November 2024
Department of Microbiology and Infection Control, University Hospital of North Norway, Tromsø, Norway.
BK polyomavirus (BKPyV) is a ubiquitous human virus that establishes a persistent infection in renal tubular epithelial cells and mainly causes disease in kidney transplant recipients. The closely related simian polyomavirus SV40 is known to cause cytoplasmic vacuolization in simian kidney cells, possibly increasing progeny release and cell death. This study aimed to determine whether BKPyV causes cytoplasmic vacuolization in primary human renal proximal tubule epithelial cells (RPTECs) and to investigate its potential role in the replication cycle.
View Article and Find Full Text PDFTumour Virus Res
December 2024
Institute of Biomedicine, University of Turku, Turku, 20520, Finland. Electronic address:
Simian virus 40 (SV40) is a monkey virus with tumorigenic potential in rodents and is associated with several types of human cancers, including lymphomas. A related Merkel cell polyomavirus causes carcinoma in humans by expressing truncated large tumor antigen (LT), with truncations caused by APOBEC family of cytidine deaminase-induced mutations. AID (activation-induced cytidine deaminase), a member of the APOBEC family, is the initiator of the antibody diversification process known as somatic hypermutation and its aberrant expression and targeting is a frequent source of lymphomagenesis.
View Article and Find Full Text PDFTransplant Proc
November 2024
Department of Surgery Nephrology Center, Toranomon Hospital, Tokyo Japan.
BK virus-associated nephritis (BKVAN) is an important cause of graft loss in renal transplant recipients B K viremia occurs in up to 30% of renal transplant recipients. Since the discovery of BKV in 1971, effective prophylaxis and treatment have not been established, and it is not uncommon for a transplant kidney to be lost without cure of BKVAN. BK virus infection is reactivated when cellular immunity is suppressed, which is often during the first year after kidney transplantation when cellular immunity is most suppressed.
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