scholarly journals The Importance of Kidney Medullary Tissue for the Accurate Diagnosis of BK Virus Allograft Nephropathy

2020 ◽  
Vol 15 (7) ◽  
pp. 1015-1023 ◽  
Author(s):  
Brian J. Nankivell ◽  
Jasveen Renthawa ◽  
Meena Shingde ◽  
Asrar Khan
Keyword(s):  
Confidence Interval ◽  
Odds Ratio ◽  
Simian Virus 40 ◽  
Estimating Equation ◽  
Simian Virus ◽  
Bk Virus ◽  
Outer Cortex ◽  
Kidney Medulla ◽  
Detection Rates ◽  
Core Length

Background and objectivesThe published tissue adequacy requirement of kidney medulla for BK virus allograft nephropathy diagnosis lacks systematic verification and competes against potential increased procedural risks from deeper sampling.Design, setting, participants, & measurementsWe evaluated whether the presence of kidney medulla improved the diagnostic rate of BK nephropathy in 2244 consecutive biopsy samples from 856 kidney transplants with detailed histologic and virologic results.ResultsMedulla was present in 821 samples (37%) and correlated with maximal core length (r=0.35; P<0.001). BK virus allograft nephropathy occurred in 74 (3% overall) but increased to 5% (42 of 821) with medulla compared with 2% (32 of 1423) for cortical samples (P<0.001). Biopsy medulla was associated with infection after comprehensive multivariable adjustment of confounders, including core length, glomerular number, and number of cores (adjusted odds ratio, 1.81; 95% confidence interval, 1.02 to 3.21; P=0.04). In viremic cases (n=275), medulla was associated with BK virus nephropathy diagnosis (39% versus 19% for cortex; P<0.001) and tissue polyomavirus load (Banff polyomavirus score 0.64±0.96 versus 0.33±1.00; P=0.006). Biopsy medulla was associated with BK virus allograft nephropathy using generalized estimating equation (odds ratio, 2.04; 95% confidence interval, 1.05 to 3.96; n=275) and propensity matched score comparison (odds ratio, 2.24; 95% confidence interval, 1.11 to 4.54; P=0.03 for 156 balanced pairs). Morphometric evaluation of Simian virus 40 large T immunohistochemistry found maximal infected tubules within the inner cortex and medullary regions (P<0.001 versus outer cortex).ConclusionsActive BK virus replication concentrated around the corticomedullary junction can explain the higher detection rates for BK virus allograft nephropathy with deep sampling. The current adequacy requirement specifying targeting medulla can be justified to minimize a missed diagnosis from undersampling.

BK Virus, JC Virus and Simian Virus 40 Infection in Humans, and Association with Human Tumors

2007 ◽  
pp. 319-341 ◽  
Author(s):  
Giuseppe Barbanti-Brodano ◽  
Silvia Sabbioni ◽  
Fernanda Martini ◽  
Massimo Negrini ◽  
Alfredo Corallini ◽  
...  
Keyword(s):  
Jc Virus ◽  
Simian Virus 40 ◽  
Simian Virus ◽  
Bk Virus ◽  
Human Tumors

Differences between BK virus and Simian Virus 40 structural proteins analysed by isoelectric focusing

1976 ◽  
Vol 51 (1-2) ◽  
pp. 163-167 ◽  
Author(s):  
G. Barbanti-Brodano ◽  
L. Lambertini ◽  
M. Tampieri ◽  
G. P. Minelli ◽  
M. Portolani ◽  
...  
Keyword(s):  
Isoelectric Focusing ◽  
Simian Virus 40 ◽  
Simian Virus ◽  
Bk Virus ◽  
Structural Proteins

scholarly journals BK Virus-Associated Nephropathy after Renal Transplantation

Pathogens ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 150
Author(s):  
Yasuhito Funahashi
Keyword(s):  
Renal Transplantation ◽  
Acute Rejection ◽  
Treatment Success ◽  
Simian Virus 40 ◽  
Simian Virus ◽  
Immunosuppressive Drugs ◽  
T Antigen ◽  
Bk Virus ◽  
Screening Tests ◽  
Urinary Cytology

Recent advances in immunosuppressive therapy have reduced the incidence of acute rejection and improved renal transplantation outcomes. Meanwhile, nephropathy caused by BK virus has become an important cause of acute or chronic graft dysfunction. The usual progression of infection begins with BK viruria and progresses to BK viremia, leading to BK virus associated nephropathy. To detect early signs of BK virus proliferation before the development of nephropathy, several screening tests are used including urinary cytology and urinary and plasma PCR. A definitive diagnosis of BK virus associated nephropathy can be achieved only histologically, typically by detecting tubulointerstitial inflammation associated with basophilic intranuclear inclusions in tubular and/or Bowman’s epithelial cells, in addition to immunostaining with anti-Simian virus 40 large T-antigen. Several pathological classifications have been proposed to categorize the severity of the disease to allow treatment strategies to be determined and treatment success to be predicted. Since no specific drugs that directly suppress the proliferation of BKV are available, the main therapeutic approach is the reduction of immunosuppressive drugs. The diagnosis of subsequent acute rejection, the definition of remission, the protocol of resuming immunosuppression, and long-term follow-up remain controversial.

scholarly journals The Agnogene of the Human Polyomavirus BK Is Expressed

1998 ◽  
Vol 72 (7) ◽  
pp. 6233-6236 ◽  
Author(s):  
Christine Hanssen Rinaldo ◽  
Terje Traavik ◽  
Allan Hey
Keyword(s):  
Simian Virus 40 ◽  
Simian Virus ◽  
Bk Virus ◽  
Human Polyomavirus ◽  
Coding Region ◽  
Reading Frame ◽  
Host Cell Proteins ◽  
Infectious Cycle ◽  
Perinuclear Area

ABSTRACT Primate polyomavirus genomes all contain an open reading frame at the 5′ end of the late coding region called the agnogene. A simian virus 40 agnoprotein with unknown functions has previously been demonstrated. We now show that a BK virus agnoprotein appears in the perinuclear area and cytoplasm late in the infectious cycle. It is phosphorylated in vivo and coimmunoprecipitates with a subset of host cell proteins.

scholarly journals Comparing Phylogenetic Codivergence between Polyomaviruses and Their Hosts

2006 ◽  
Vol 80 (12) ◽  
pp. 5663-5669 ◽  
Author(s):  
Marcos Pérez-Losada ◽  
Ryan G. Christensen ◽  
David A. McClellan ◽  
Byron J. Adams ◽  
Raphael P. Viscidi ◽  
...  
Keyword(s):  
Bayesian Methods ◽  
Evolutionary History ◽  
Simian Virus 40 ◽  
Simian Virus ◽  
Bk Virus ◽  
Hamster Polyomavirus ◽  
Reconciliation Analysis ◽  
History Of ◽  
Bovine Polyomavirus ◽  
Avian Polyomavirus

ABSTRACT Seventy-two full genomes corresponding to nine mammalian (67 strains) and two avian (5 strains) polyomavirus species were analyzed using maximum likelihood and Bayesian methods of phylogenetic inference. Our fully resolved and well-supported (bootstrap proportions > 90%; posterior probabilities = 1.0) trees separate the bird polyomaviruses (avian polyomavirus and goose hemorrhagic polyomavirus) from the mammalian polyomaviruses, which supports the idea of spitting the genus into two subgenera. Such a split is also consistent with the different viral life strategies of each group. Simian (simian virus 40, simian agent 12 [Sa12], and lymphotropic polyomavirus) and rodent (hamster polyomavirus, mouse polyomavirus, and murine pneumotropic polyomavirus [MPtV]) polyomaviruses did not form monophyletic groups. Using our best hypothesis of polyomavirus evolutionary relationships and established host phylogenies, we performed a cophylogenetic reconciliation analysis of codivergence. Our analyses generated six optimal cophylogenetic scenarios of coevolution, including 12 codivergence events (P< 0.01), suggesting that Polyomaviridae coevolved with their avian and mammal hosts. As individual lineages, our analyses showed evidence of host switching in four terminal branches leading to MPtV, bovine polyomavirus, Sa12, and BK virus, suggesting a combination of vertical and horizontal transfer in the evolutionary history of the polyomaviruses.

scholarly journals Prevalence and stability of human serum antibodies to simian virus 40 VP1 virus-like particles

2005 ◽  
Vol 86 (6) ◽  
pp. 1703-1708 ◽  
Author(s):  
Annika Lundstig ◽  
Linda Eliasson ◽  
Matti Lehtinen ◽  
Kestutis Sasnauskas ◽  
Pentti Koskela ◽  
...  
Keyword(s):  
Jc Virus ◽  
Simian Virus 40 ◽  
Simian Virus ◽  
Bk Virus ◽  
Confirmatory Test ◽  
Human Populations ◽  
Specific Antibodies ◽  
Virus Like Particles ◽  
Sv40 Dna ◽  
Over Time

Possible human infection with simian virus 40 (SV40) has been of great concern ever since SV40 was discovered in polio vaccines. Human populations are SV40-seropositive, but because of serological cross-reactivity between SV40 and the human polyomaviruses BK virus (BKV) and JC virus (JCV), it is debatable whether these antibodies are specific. An SV40-specific serological assay was established, based on purified virus-like particles (VLPs), where the SV40 VLPs were blocked with hyperimmune sera to BKV and JCV. Competition with SV40 hyperimmune sera was used as a confirmatory test. Among 288 Swedish children of between 1 and 13 years of age, 7·6 % had SV40-specific antibodies. SV40 seroprevalence reached a peak of 14 % at 7–9 years of age. Among 100 control patients with benign tumours, 9 % were SV40-seropositive. However, SV40 DNA was not detectable in corresponding buffy-coat samples. In serial samples taken up to 5 years apart from 141 Finnish women participating in the population-based serological screening for congenital infections, only two of 141 women were SV40-seropositive in both samples. Six women seroconverted and eight women had a loss of antibodies over time. None of the SV40-seropositive samples contained detectable SV40 DNA. In conclusion, there is a low prevalence of SV40-specific antibodies in the Nordic population. The SV40 antibodies appear to have a low stability over time and their origin is not clear.

scholarly journals Comparison of Antibody Titers Determined by Hemagglutination Inhibition and Enzyme Immunoassay for JC Virus and BK Virus

2000 ◽  
Vol 38 (1) ◽  
pp. 105-109
Author(s):  
R. S. Hamilton ◽  
M. Gravell ◽  
E. O. Major
Keyword(s):  
Enzyme Immunoassay ◽  
Hemagglutination Inhibition ◽  
Jc Virus ◽  
Simian Virus 40 ◽  
Simian Virus ◽  
Bk Virus ◽  
Reciprocal Relationship ◽  
High Antibody ◽  
Dot Blot ◽  
Antibody Titers

ABSTRACT A comparison of antibody titers to JC virus (JCV) or BK virus (BKV) was made by hemagglutination inhibition (HI) and enzyme immunoassay (EIA) with 114 human plasma samples. Antibody titers to JCV or BKV determined by HI were lower than those determined by EIA. Nevertheless, as HI titers increased so did EIA titers. When antibody data were compared by the Spearman rank correlation test, highly significant correlations were found between HI and EIA titers. Results obtained by plotting EIA antibody titers for JCV against those for BKV generally showed a reciprocal relationship, i.e., samples with high antibody titers to JCV had lower antibody titers to BKV and vice versa. Some samples, however, had antibody titers to both viruses. Of the samples tested, 25.4% (25 of 114) had HI and EIA antibody titers to JCV and BKV which were identical or closely related. This is not the scenario one would expect for cross-reactive epitopes shared by the two viruses, but one suggesting that these samples were from individuals who had experienced infections by both viruses. Adsorption with concentrated JCV or BKV antigen of sera with high antibody titers to both JCV and BKV and testing by JCV and BKV EIA gave results which support this conclusion. Although 52.6% (51 of 97) of the samples from the Japanese population tested had very high antibody titers (≥40,960) to either JCV or BKV, none of the samples were found by a dot blot immunoassay to have antibodies which cross-reacted with simian virus 40. The results from this study, in agreement with those of others, suggest that humans infected by JCV or BKV produce antibodies to species-specific epitopes on their VP1 capsid protein, which is associated with hemagglutination and cellular binding.

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