ライフサイエンスコーパス: BKV

1 BKV and JCV were commonly detected in the urine of lung

2 BKV and mouse polyomavirus were used to infect human and

3 BKV DNA surveillance was performed at 1, 3, 6, 12, and 2

4 BKV enters HRPTEC by caveolar-mediated endocytosis.

5 BKV genotype-specific NAb titers may be a meaningful pre

6 BKV infection of primary human TEC did not induce an ant

7 BKV infection progresses to BKV nephritis (BKVN) in appr

8 BKV infection was associated with poorer survival.

9 BKV reactivation in immunosuppressed patients or renal t

10 BKV replication was quantified by measurement of urinary

11 BKV serostatus can be used to risk stratify patients for

12 BKV specifically evades innate immunity in TEC and is no

13 BKV subtype III is rarely identified and has not previou

14 BKV subtype IV had a higher prevalence in recipients wit

15 BKV subtype IV may be one of the viral determinants.

16 BKV viremia was observed in 20% of the desensitized and

17 BKV viremia was observed in 20% of the desensitized and

18 BKV was monitored every 2 months in the urine or blood.

19 BKV whole genomes were amplified using long-range PCR wi

20 Prototype 1 (BKV Dun) could be reliably detected at concentrations as

21 th a minority before (7.8%) or after (40.1%) BKV clearance.

22 uses, including simian vacuolating virus 40, BKV, and JCV.

23 reviously reported cutoff value of 6.5x10(5) BKV viral capsid protein 1 (VP-1) mRNA/ng RNA in urinary

24 aried significantly among viruses: JCV, 64%; BKV, 48%; and SV40, 14%.

25 ignaling pathways that target them) activate BKV replication and contribute to the consequent patholo

26 f 37.0 (P=0.1216) after resolution of active BKV infection.

27 of BKVN and then after resolution of active BKV infection.

28 ation of fluoroquinolone prophylaxis against BKV infection remain unknown.

29 appear to be markers for protection against BKV infection (OR: 0.29, 95% CI: 0.1-0.83, P=0.01 for rs

30 ne prophylaxis directed specifically against BKV has not been formally tested against a control group

31 However, consistent detection of all BKV variants was possible only at concentrations of 10,0

32 P-10, cytotoxic perforin and granzyme B, and BKV VP1 mRNA were not different (P>0.05) between HIV-inf

33 tigated the urine virome profile of BKV+ and BKV- kidney transplant recipients.

34 ntitative viral replication of CMV, EBV, and BKV in oral washes, urine, and whole blood pretransplant

35 and 65.5% for the detection of CMV, EBV, and BKV, respectively.

36 n a state of increased immunosuppression and BKV infection, especially in patients with higher MMF ex

37 e the structure-based design of dual JCV and BKV ATP-competitive inhibitors.

38 tions caused by human polyomaviruses JCV and BKV.

39 a risk factor for subsequent BKV viremia and BKV-associated nephropathy.

40 Any BKV infection developed in 25 of 41, 22 of 42, 17 of 41,

41 ], and D-R- [n=68]), 89 of 192 developed any BKV infection and 62 of 89 developed BK insignificant vi

42 ic regression model showed lower risk of any BKV infection in African American recipient race (OR, 0.

43 The outcomes studied were development of any BKV infection, viremia, and significant viremia (>/=10,0

44 As BKV-specific treatments are limited, immunologic-based t

45 ia and 25 had significant viremia defined as BKV DNA more than 10,000 copies/mL of plasma.

46 entify BKV variants across the genome and at BKV-specific HLA-A2-, HLA-B0702-, and HLA-B08-restricted

47 f mice given virus-like particle (VLP)-based BKV vaccines confirmed these findings.

48 KV nephropathy group, urine and blood became BKV positive earlier than in the group with viruria and

49 these results support an association between BKV and urothelial carcinogenesis among kidney transplan

50 Here we investigated the interplay between BKV and TEC in more detail.

51 Reactivation of polyomavirus BK (BKV) after renal transplantation can lead to allograft d

52 Knowledge of polyomavirus BK (BKV) genomic diversity has greatly expanded.

53 Polyomavirus BK (BKV) infection can cause nephropathy in the allograft ki

54 Polyomavirus BK (BKV) infection characterized by viruria alone is conside

55 ation increases the risk of polyomavirus BK (BKV) viremia.

56 ation increases the risk of polyomavirus BK (BKV) viremia.

57 marker that allows patient stratification by BKV disease risk before and after transplant.

58 as quantified by measurement of urinary cell BKV VP1 mRNA levels using BKV specific primers and TaqMa

59 of renal function and prevention of clinical BKV nephritis and graft loss.

60 Comparing BKV subtypes of donor and recipient before with the subt

61 Human IVIG preparations contain BKV neutralizing antibodies.

62 In contrast, BKV infection of leukocytes did elicit an antiviral resp

63 of caveolin-1, prevented caveolar-dependent BKV internalization and repressed BKV infection of HRPTE

64 Donor-derived BKV transmission is an important mode of infection.

65 Together with reports describing BKV detection in tumor tissues, these results support an

66 y two patients (8.7%) with UC had detectable BKV.

67 A surveillance strategy for detecting BKV reactivation based on urine cytology is cost-effecti

68 A total of 94 developed BKV infection (any degree of BK viruria or viremia) wher

69 er proportion of African Americans developed BKV infection, 14 of 61 (23%), as opposed to whites, 67

70 arison of Altona with a laboratory-developed BKV NAAT assay in IU/ml versus copies/ml using Passing-B

71 cating strain had a lower risk of developing BKV viremia (hazard ratio [HR], 0.44; 95% confidence int

72 tional unit (IU) using the Exact Diagnostics BKV verification panel, a secondary standard traceable t

73 The finding implies that different BKV genotypes have different cellular tropisms and patho

74 fter transplant, 52 (31%) patients displayed BKV replication: 24 (46%) patients were viruric and 28 (

75 orter pseudoviruses based on seven divergent BKV isolates and performed neutralization assays on sera

76 Donor BKV replication occurred in 17%, mostly in the urine and

77 Early BKV positivity of urine and blood indicates later BKV ne

78 donor transmission in 95% of cases of early BKV replication.

79 ellular immune response to peptides encoding BKV large T antigen.

80 Decreased renal function may favor BKV infection.

81 For BKV prototypes with 2 or more mismatches (representing g

82 l and the following rates by virus: 100% for BKV (n = 16), 94% for CMV (n = 17), 71% for AdV (n = 7),

83 ecipients from January 2007 to June 2011 for BKV and/or CMV viremia.

84 least once, including 38 patients (42%) for BKV, 25 patients (28%) for JCV, and six patients (7%) fo

85 as a previously unrecognized risk factor for BKV reactivation after renal transplantation.

86 mia or viruria, analysis of risk factors for BKV nephritis as an endpoint could lead to erroneous fin

87 te globulin are independent risk factors for BKV replication in renal allograft recipients treated wi

88 ent of BK viremia, specific risk factors for BKV-related complications in the transplant setting rema

89 /L (AHR, 3.6; P=0.001) were risk factors for BKV.

90 Urinary viral loads for BKV (10 copies/mL) and JCV (10 copies/mL) were higher th

91 body (NAb) titers as a predictive marker for BKV replication, we measured BKV DNA load and NAb titers

92 in the presence of viruria but negative for BKV stains were designated as putative T-cell-mediated a

93 fer certain protection or predisposition for BKV infection.

94 hese data indicate that NFAT is required for BKV infection and is involved in a complex regulatory ne

95 ciated with a significantly reduced risk for BKV infection (OR: 0.43, 95% CI: 0.25-0.73, P=0.001).

96 nt recipients may identify those at risk for BKV-associated nephropathy.

97 The 1st WHO International Standard for BKV (primary standard) was introduced in 2016 as a commo

98 More frequent surveillance for BKV viremia and an early, aggressive treatment strategy

99 More frequent surveillance for BKV viremia and an early, aggressive treatment strategy

100 Surveillance for BKV viremia was done at 1, 2, 3, 6, 9, and 12 months pos

101 Surveillance for BKV viremia was done at 1, 2, 3, 6, 9, and 12 months pos

102 e feasible by measurement of transcripts for BKV viral capsid protein 1 (VP-1), GB, and PI-9 in urine

103 Thirteen of 14 patients treated for BKV-associated hemorrhagic cystitis experienced complete

104 is shows a trend toward greater freedom from BKV infection in African Americans as opposed to other r

105 After repeat transplant, 11 (35%) had BKV replication in urine and plasma with two patients ex

106 A was undetectable at 24 months and none had BKV replication.

107 While nearly all healthy subjects had BKV genotype I-neutralizing antibodies, a majority of su

108 aceable to the primary standard to harmonize BKV NAAT results, we anticipate improved interassay comp

109 Here, BKV viremia in HLA-sensitized patients after desensitiza

110 Here, BKV viremia in HLA-sensitized patients after desensitiza

111 t strategy are essential for preventing high BKV viral loads in this patient population.

112 t strategy are essential for preventing high BKV viral loads in this patient population.

113 However, BKV infection did not affect dsDNA-induced gene expressi

114 gy and bioinformatics pipeline that identify BKV variants across the genome and at BKV-specific HLA-A

115 e the whole-genome sequence of a subtype III BKV from a pediatric kidney transplant patient with poly

116 amine the role of antimicrobial defensins in BKV infection of Vero cells.

117 ever, there was no significant difference in BKV-associated nephropathy or graft loss in the two grou

118 ever, there was no significant difference in BKV-associated nephropathy or graft loss in the two grou

119 (NFAT) plays an important regulatory role in BKV infection.

120 The function of the innate immune system in BKV infection and pathology has not been investigated.

121 Renal function was worse in BKV-nephropathy compared with BKV-negative patients begi

122 ct dsDNA-induced gene expression, indicating BKV did not modulate the antiviral response.

123 ors (D)-recipient (R) pairs using infectious BKV neutralization assays with representatives from the

124 Fluoroquinolones inhibit BKV replication in vitro, and small studies suggest in v

125 P1) and human alpha-defensin 5 (HD5) inhibit BKV infection by targeting an early event in the viral l

126 ion of certain misfolded proteins, inhibited BKV infection.

127 competition with templates containing intact BKV NCCRs.

128 present the outcomes from an early intensive BKV surveillance program using decoy cell detection for

129 It was found that currently known BKV subtypes and subgroups can no longer be reliably det

130 viridae: Aichi virus (AV), bovine kobuvirus (BKV), canine kobuvirus (CKoV), mouse kobuvirus (MKoV), s

131 The distribution of purified and labeled BKV particles in the presence and absence of pravastatin

132 d interfered with internalization of labeled BKV particles.

133 ositivity of urine and blood indicates later BKV nephropathy.

134 different standards to prospectively measure BKV titers in 251 urine specimens submitted to our clini

135 tive marker for BKV replication, we measured BKV DNA load and NAb titers at transplant and followed p

136 gan transplant recipients with a multivalent BKV VLP vaccine might reduce the risk of developing post

137 e in antibiotic prophylaxis practice from no BKV prophylaxis (Group 1, n=106, July-December 2009) to

138 were evaluated in three eras: (i) Era-I: No BKV PCR performed (n = 36), (ii) Era-II: PCR performed f

139 significantly associated with the absence of BKV replication after repeat transplantation.

140 The activation of BKV replication following kidney transplantation, leadin

141 There was an association of BKV viremia with desensitization and lymphocyte inductio

142 There was an association of BKV viremia with desensitization and lymphocyte inductio

143 nce and regulatory micro (mi)RNA clusters of BKV, JCV and SV40.

144 Coincubation of BKV but not mouse polyomavirus with clinically relevant

145 source and factors influencing the course of BKV infection.

146 The sensitivity of detection of BKV in the PCR assay was a function of the viral genotyp

147 Detection of BKV infection very early (ie, 5 days) after transplantat

148 41%, respectively, from time of diagnosis of BKV infection to complete resolution of viremia.

149 mbers interacted with the helicase domain of BKV Tag in pulldown assays, suggesting that NFI helps re

150 ore and after transplantation; genotyping of BKV subtypes was performed.

151 alibrator for improving the harmonization of BKV nucleic acid amplification testing (NAAT) and enabli

152 The implications of BKV DNA sequence variation for the performance of molecu

153 The incidence of BKV infection in the total population was 163 of 609 (26

154 mab is associated with a higher incidence of BKV viremia with high viral copies and was the major pre

155 mab is associated with a higher incidence of BKV viremia with high viral copies and was the major pre

156 applicable thresholds for the management of BKV infection in transplantation.

157 luate the risk factors for the occurrence of BKV infections using BK viruria and viremia as endpoints

158 ucted to determine incidence and outcomes of BKV infection.

159 Both the percentage of BKV infected cells and the large T-antigen expression we

160 viral copies and was the major predictor of BKV viremia in the multivariable model.

161 viral copies and was the major predictor of BKV viremia in the multivariable model.

162 ansplantation and tested for the presence of BKV by polymerase chain reaction.

163 ents were tested by qPCR for the presence of BKV DNA before and after transplantation; genotyping of

164 The prevalence of BKV replication increased over time and was highest at 6

165 we investigated the urine virome profile of BKV+ and BKV- kidney transplant recipients.

166 ecipients is associated with a lower rate of BKV infection at 3 months but not at 12 months.

167 We hypothesize that the rate of BKV infection can be curbed by competitively preventing

168 2, n=130, January-June 2010) on the rate of BKV infection during the first 12 months after kidney tr

169 were significantly higher incidence rates of BKV viruria, Pneumocystis jiroveci pneumonia, and malign

170 The replication of BKV DNA in cell cultures is regulated by the viral nonco

171 alpha or dsDNA did not hamper replication of BKV, whereas influenza and herpes simplex virus 1 replic

172 tatus may be useful in assessing the risk of BKV infection in kidney transplant recipients.

173 hylprednisolone did not increase the risk of BKV replication.

174 so investigated the risk factors and role of BKV in the carcinogenesis of de novo UC by quantitative

175 Using the Dunlop strain of BKV, we found that nuclear factor of activated T cells (

176 oads were significantly higher than those of BKV in both patient groups (P< .0001).

177 To assess the value of BKV genotype-specific neutralizing antibody (NAb) titers

178 sialogangliosides, which bind to the VP1 of BKV, also associate with our BKV template.

179 as found in the viral coat protein, VP1, of BKV.

180 Based on BKV-specific IgG enzyme immunoassay >/=8 units, subjects

181 Individuals who are infected with one BKV serotype may remain humorally vulnerable to other BK

182 ype may remain humorally vulnerable to other BKV serotypes after implementation of T cell immunosuppr

183 d to the VP1 of BKV, also associate with our BKV template.

184 on for transplant recipients with persistent BKV infection.

185 At time of diagnosis, mean plasma BKV DNA (copies/mL) was 460,409 (range 10,205-1,920,691)

186 The mean plasma BKV DNA declined by 98% (range, 76%-100%) at 1 year afte

187 stein-Barr virus (EBV), and BK polyomavirus (BKV) at transplant was a risk factor for posttransplant

188 BK polyomavirus (BKV) causes significant urinary tract pathogenesis in im

189 BK polyomavirus (BKV) establishes persistent, low-level, and asymptomatic

190 kidney transplant patients, BK polyomavirus (BKV) has been shown to induce nephropathy (BKVN), decrea

191 eries describe detection of BK polyomavirus (BKV) in urinary tract cancers in kidney transplant recip

192 The pathogenesis of BK polyomavirus (BKV) infection and associated nephropathy in renal trans

193 BK polyomavirus (BKV) infection remains a significant cause of nephropath

194 BK polyomavirus (BKV) is an emerging pathogen in immunocompromised indivi

195 BK polyomavirus (BKV)-associated nephropathy is a threat to kidney allogr

196 quency of urinary shedding of polyomaviruses BKV and JCV and their relationship to creatinine clearan

197 reduce the risk of developing posttransplant BKV disease.

198 ican race had a lower risk of posttransplant BKV infection compared with whites, independent of other

199 o evaluate various aspects of posttransplant BKV infection.

200 recipient serostatus to posttransplantation BKV infection.

201 ients with or without treatment for presumed BKV nephropathy (tBKVN) using data from the United State

202 retrospectively determined the pretransplant BKV neutralizing serostatus of 116 donors (D)-recipient

203 Pretransplantation BKV serostatus was available for 192 adult and 11 pediat

204 cells (HRPTEC) and, correspondently, prevent BKV infection.

205 tralizing antibodies can moderate or prevent BKV disease.

206 omes, acute rejection rate, HIV progression, BKV replication, infections, and urinary cell mRNA profi

207 end toward higher incidence of biopsy-proven BKV nephropathy in Group 1 (4.7% vs. 0.8%, P=0.057).

208 HCT and kidney recipients with quantifiable BKV DNAemia underwent whole-genome sequencing.

209 This included 7453 quantitative BKV polymerase chain reaction and 15,496 quantitative CM

210 establishing broadly applicable quantitative BKV DNA load cutoffs for clinical practice.

211 Here, we evaluated the Altona RealStar BKV assay (Altona) and calibrated the results to the int

212 BKV replication is associated with recipient BKV viremia in kidney transplants.

213 ion, either individually or in toto, reduces BKV DNA replication when placed in competition with temp

214 red T-cell epitopes similar to the reference BKV strain that was matched for the BKV genotype.

215 ed to treat hypercholesterolemia, to repress BKV entry pathways in human renal proximal tubular epith

216 -dependent BKV internalization and repressed BKV infection of HRPTEC.

217 Clinically significant BKV reactivation occurs early after transplantation and

218 .82; P=0.016) and higher risk of significant BKV infection with occurrence of acute rejection (OR, 3.

219 ies of NFI: the NFIC/CTF1 isotype stimulates BKV template replication in vitro at low concentrations

220 underwent biopsy presented with subclinical BKV nephritis.

221 s identified as a risk factor for subsequent BKV viremia and BKV-associated nephropathy.

222 nts demonstrated a higher rate of subsequent BKV viremia than patients with antecedent CMV viremia (P

223 d large T-antigen expression which suggested BKV infection by Western blots was assessed in the absen

224 Surprisingly, BKV subgenotypes Ib1 and Ib2 can behave as fully distinc

225 s that potently cross-neutralized all tested BKV genotypes.

226 The results demonstrate that BKV genotypes I, II, III, and IV are fully distinct sero

227 Our results demonstrate that BKV infection in RPTE cells involves an acidic environme

228 These results indicate that BKV early entry and disassembly are highly regulated pro

229 These findings suggest that BKV and JCV display different patterns of reactivation a

230 idney transplant recipients, suggesting that BKV could contribute to the development of these cancers

231 ly available VP-1 sequences encompassing the BKV genomic region targeted by an in-house quantitative

232 eference BKV strain that was matched for the BKV genotype.

233 In the BKV nephropathy group, urine and blood became BKV positi

234 While the BK virus was predominant in the BKV+ group, it was also found in the BKV- group patients

235 in the BKV+ group, it was also found in the BKV- group patients.

236 Analysis of the BKV subtypes showed that nucleotide polymorphisms were d

237 tingly, we detected multiple subtypes of the BKV, JCV and TTV.

238 These data demonstrate that the BKV template mimics the host cell binding observed for t

239 axis (Group 1, n=106, July-December 2009) to BKV prophylaxis with ciprofloxacin 250 mg twice daily fo

240 show a novel mechanism whereby HD5 binds to BKV leading to aggregation of virion particles preventin

241 No grafts were lost due to BKV during the study period.

242 w that proteasome function is also linked to BKV infection and capsid rearrangement.

243 BKV infection progresses to BKV nephritis (BKVN) in approximately 8% of transplants

244 nificantly associated with susceptibility to BKV infection (OR: 2.9, 95% CI: 1.29-6.44, P=0.007) whil

245 P=0.02), and a significantly shorter time to BKV viremia (P=0.01) in kidney recipients.

246 cells (TEC) show a limited response towards BKV infection.

247 Donor urinary BKV replication is associated with recipient BKV viremia

248 Pretransplant urinary BKV shedding of donor and recipient is a risk for posttr

249 Pretransplant urinary BKV shedding of donor or recipient was a significant ris

250 ciated with posttransplant recipient urinary BKV replication in recipients, it was associated with BK

251 nt of urinary cell BKV VP1 mRNA levels using BKV specific primers and TaqMan probe in a real-time qua

252 In conclusion, variant BKV strains lower the sensitivity of detection and may h

253 only two disease-causing members (BK virus (BKV) and JC virus (JCV)) identified.

254 riability in the quantification of BK virus (BKV) DNA precludes establishing broadly applicable thres

255 Quantitative BK virus (BKV) DNA surveillance in plasma/urine was performed at 1

256 ransplant recipients, particularly BK virus (BKV) in kidney transplant patients.

257 the detection and the role of the BK virus (BKV) in the carcinogenesis of urothelial carcinoma (UC)

258 imited data on the epidemiology of BK virus (BKV) infection after alemtuzumab induction.

259 BK virus (BKV) infection causing end-organ disease remains a formi

260 BK virus (BKV) infection of kidney transplant patients is an incre

261 widely recognized risk factor for BK virus (BKV) infection, particularly with the combination of tac

262 Cytomegalovirus (CMV) and BK virus (BKV) infections can cause significant morbidity after ki

263 The human polyomavirus BK virus (BKV) is a common virus for which 80 to 90% of the adult

264 BK virus (BKV) is a polyomavirus that establishes a lifelong persi

265 Because the occurrence of BK virus (BKV) nephritis is far less frequent than BK viremia or v

266 BK virus (BKV) nephropathy remains the main cause of renal graft l

267 Identification of risk factors for BK virus (BKV) replication may improve transplant outcome.

268 case of the human polyomaviruses, BK virus (BKV) replication occurs in the tubular epithelial cells

269 s (CMV), Epstein-Barr virus (EBV), BK virus (BKV), adenovirus (ADV), and human herpesvirus 6 (HHV6) w

270 irus (AdV), cytomegalovirus (CMV), BK virus (BKV), and human herpesvirus 6 (HHV-6).

271 Samples were analyzed for BK virus (BKV), JC virus (JCV), and simian virus 40 (SV40) by conv

272 BK virus (BKV)-associated nephropathy is the second leading cause

273 relationship of pretransplantation BK virus (BKV)-specific donor and recipient serostatus to posttran

274 rr virus (EBV), and 64 (34.6%) for BK virus (BKV).

275 MV), Epstein-Barr virus (EBV), and BK virus (BKV).

276 quent detection of polyomaviruses (BK virus [BKV] or simian virus 40 [SV40]) in 46% of stool samples

277 HSCT, including infections from two viruses (BKV and HHV-6) that had never been targeted previously w

278 than kidney recipients (71% vs 38%), whereas BKV was shed more often by kidney than liver patients (6

279 KoV also contain these four domains, whereas BKV, SKV, and TV2/TV3 5' UTRs contain domains that are r

280 In particular, we questioned whether BKV suppresses and/or evades antiviral responses.

281 It is currently unclear whether BKV-neutralizing antibodies can moderate or prevent BKV

282 core origin and flanking sequences, to which BKV T antigen (Tag), cellular proteins, and small regula

283 re positive for human polyomaviruses: 9 with BKV, 9 with JC virus (JCV), 1 with SV40, and 1 with both

284 Risk factors associated with BKV infection in univariate analyses were retransplantat

285 IFN-gamma polymorphisms are associated with BKV infection.

286 ore transplant significantly associated with BKV replication after transplant (HR, 1.88; 95% CI, 1.06

287 cation in recipients, it was associated with BKV viremia (P=0.02), and a significantly shorter time t

288 n was worse in BKV-nephropathy compared with BKV-negative patients beginning at transplantation.

289 Then the percentage of HRPTEC infected with BKV by immunofluorescent analysis and large T-antigen ex

290 l blood mononuclear cells were infected with BKV Dunlop strain or other viruses.

291 high prevalence of persistent infection with BKV in the general population, it is possible that eithe

292 Reduced survival was noted for patients with BKV infection (P=0.03).

293 hose without infection, but in patients with BKV infection, creatinine clearances were lower at times

294 to validate the use of IVIG in patients with BKV infection.

295 even on a separate analysis of patients with BKV load 1E+07 copies per mL or less.

296 nificantly higher at 1 year in patients with BKV replication.

297 V had a higher prevalence in recipients with BKV nephropathy than in those with viruria and viremia (

298 ected from a total of 251 RTRs (71 RTRs with BKV infection and 180 without BKV infection).

299 recipients at our center were screened with BKV plasma PCR monthly for the first 4 months posttransp

300 (71 RTRs with BKV infection and 180 without BKV infection).