Presence, quantitation and characterization of JC virus in the urine of Italian immunocompetent subjects
Human polyomavirus JC (JCV) infects the worldwide population, remains latent in the kidney, and is excreted in the urine. A longitudinal study was performed in order to evaluate JCV excretion, to characterize molecularly the virus and to determine if its presence in urine is a consequence of viral r...
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| Published in | Journal of medical virology Vol. 79; no. 4; pp. 408 - 412 |
|---|---|
| Main Authors | , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Hoboken
Wiley Subscription Services, Inc., A Wiley Company
01.04.2007
Wiley-Liss |
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| Online Access | Get full text |
| ISSN | 0146-6615 1096-9071 |
| DOI | 10.1002/jmv.20829 |
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| Abstract | Human polyomavirus JC (JCV) infects the worldwide population, remains latent in the kidney, and is excreted in the urine. A longitudinal study was performed in order to evaluate JCV excretion, to characterize molecularly the virus and to determine if its presence in urine is a consequence of viral reactivation or merely of epithelial squamous cell shedding. The presence of cellular sediment and the JCV genome were examined in 333 urine samples collected periodically for 3 months from 17 healthy subjects; molecular characterization, and quantitation of the virus were also undertaken. JCV DNA was detected in 40.2% of the samples, with a significant difference (P < 0.001) observed between males and females. JCV shedding was independent of the presence of cellular sediment in every individual. JCV genotype 1 was the genome detected most frequently, while all of the amplified strains showed archetypal organization of the transcriptional control region (TCR). No clinical symptoms have been associated with JCV excretion and no microbial load was detected in the urine samples. The lack of correlation between JCV DNA detection and the presence of squamous cells in urine sediment indicates that viruria is regulated by the life cycle of JCV. Thus, the virus is eliminated as consequence of its reactivation. J. Med. Virol. 79:408–412, 2007. © 2007 Wiley‐Liss, Inc. |
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| AbstractList | Human polyomavirus JC (JCV) infects the worldwide population, remains latent in the kidney, and is excreted in the urine. A longitudinal study was performed in order to evaluate JCV excretion, to characterize molecularly the virus and to determine if its presence in urine is a consequence of viral reactivation or merely of epithelial squamous cell shedding. The presence of cellular sediment and the JCV genome were examined in 333 urine samples collected periodically for 3 months from 17 healthy subjects; molecular characterization, and quantitation of the virus were also undertaken. JCV DNA was detected in 40.2% of the samples, with a significant difference (
P
< 0.001) observed between males and females. JCV shedding was independent of the presence of cellular sediment in every individual. JCV genotype 1 was the genome detected most frequently, while all of the amplified strains showed archetypal organization of the transcriptional control region (TCR). No clinical symptoms have been associated with JCV excretion and no microbial load was detected in the urine samples. The lack of correlation between JCV DNA detection and the presence of squamous cells in urine sediment indicates that viruria is regulated by the life cycle of JCV. Thus, the virus is eliminated as consequence of its reactivation. J. Med. Virol. 79:408–412, 2007. © 2007 Wiley‐Liss, Inc. Human polyomavirus JC (JCV) infects the worldwide population, remains latent in the kidney, and is excreted in the urine. A longitudinal study was performed in order to evaluate JCV excretion, to characterize molecularly the virus and to determine if its presence in urine is a consequence of viral reactivation or merely of epithelial squamous cell shedding. The presence of cellular sediment and the JCV genome were examined in 333 urine samples collected periodically for 3 months from 17 healthy subjects; molecular characterization, and quantitation of the virus were also undertaken. JCV DNA was detected in 40.2% of the samples, with a significant difference (P<0.001) observed between males and females. JCV shedding was independent of the presence of cellular sediment in every individual. JCV genotype 1 was the genome detected most frequently, while all of the amplified strains showed archetypal organization of the transcriptional control region (TCR). No clinical symptoms have been associated with JCV excretion and no microbial load was detected in the urine samples. The lack of correlation between JCV DNA detection and the presence of squamous cells in urine sediment indicates that viruria is regulated by the life cycle of JCV. Thus, the virus is eliminated as consequence of its reactivation. J. Med. Virol. 79:408-412, 2007. Human polyomavirus JC (JCV) infects the worldwide population, remains latent in the kidney, and is excreted in the urine. A longitudinal study was performed in order to evaluate JCV excretion, to characterize molecularly the virus and to determine if its presence in urine is a consequence of viral reactivation or merely of epithelial squamous cell shedding. The presence of cellular sediment and the JCV genome were examined in 333 urine samples collected periodically for 3 months from 17 healthy subjects; molecular characterization, and quantitation of the virus were also undertaken. JCV DNA was detected in 40.2% of the samples, with a significant difference (P < 0.001) observed between males and females. JCV shedding was independent of the presence of cellular sediment in every individual. JCV genotype 1 was the genome detected most frequently, while all of the amplified strains showed archetypal organization of the transcriptional control region (TCR). No clinical symptoms have been associated with JCV excretion and no microbial load was detected in the urine samples. The lack of correlation between JCV DNA detection and the presence of squamous cells in urine sediment indicates that viruria is regulated by the life cycle of JCV. Thus, the virus is eliminated as consequence of its reactivation. J. Med. Virol. 79:408–412, 2007. © 2007 Wiley‐Liss, Inc. Human polyomavirus JC (JCV) infects the worldwide population, remains latent in the kidney, and is excreted in the urine. A longitudinal study was performed in order to evaluate JCV excretion, to characterize molecularly the virus and to determine if its presence in urine is a consequence of viral reactivation or merely of epithelial squamous cell shedding. The presence of cellular sediment and the JCV genome were examined in 333 urine samples collected periodically for 3 months from 17 healthy subjects; molecular characterization, and quantitation of the virus were also undertaken. JCV DNA was detected in 40.2% of the samples, with a significant difference (P<0.001) observed between males and females. JCV shedding was independent of the presence of cellular sediment in every individual. JCV genotype 1 was the genome detected most frequently, while all of the amplified strains showed archetypal organization of the transcriptional control region (TCR). No clinical symptoms have been associated with JCV excretion and no microbial load was detected in the urine samples. The lack of correlation between JCV DNA detection and the presence of squamous cells in urine sediment indicates that viruria is regulated by the life cycle of JCV. Thus, the virus is eliminated as consequence of its reactivation. Human polyomavirus JC (JCV) infects the worldwide population, remains latent in the kidney, and is excreted in the urine. A longitudinal study was performed in order to evaluate JCV excretion, to characterize molecularly the virus and to determine if its presence in urine is a consequence of viral reactivation or merely of epithelial squamous cell shedding. The presence of cellular sediment and the JCV genome were examined in 333 urine samples collected periodically for 3 months from 17 healthy subjects; molecular characterization, and quantitation of the virus were also undertaken. JCV DNA was detected in 40.2% of the samples, with a significant difference (P<0.001) observed between males and females. JCV shedding was independent of the presence of cellular sediment in every individual. JCV genotype 1 was the genome detected most frequently, while all of the amplified strains showed archetypal organization of the transcriptional control region (TCR). No clinical symptoms have been associated with JCV excretion and no microbial load was detected in the urine samples. The lack of correlation between JCV DNA detection and the presence of squamous cells in urine sediment indicates that viruria is regulated by the life cycle of JCV. Thus, the virus is eliminated as consequence of its reactivation.Human polyomavirus JC (JCV) infects the worldwide population, remains latent in the kidney, and is excreted in the urine. A longitudinal study was performed in order to evaluate JCV excretion, to characterize molecularly the virus and to determine if its presence in urine is a consequence of viral reactivation or merely of epithelial squamous cell shedding. The presence of cellular sediment and the JCV genome were examined in 333 urine samples collected periodically for 3 months from 17 healthy subjects; molecular characterization, and quantitation of the virus were also undertaken. JCV DNA was detected in 40.2% of the samples, with a significant difference (P<0.001) observed between males and females. JCV shedding was independent of the presence of cellular sediment in every individual. JCV genotype 1 was the genome detected most frequently, while all of the amplified strains showed archetypal organization of the transcriptional control region (TCR). No clinical symptoms have been associated with JCV excretion and no microbial load was detected in the urine samples. The lack of correlation between JCV DNA detection and the presence of squamous cells in urine sediment indicates that viruria is regulated by the life cycle of JCV. Thus, the virus is eliminated as consequence of its reactivation. |
| Author | Valli, Marilena Ferrante, Pasquale Mancuso, Roberta Calvo, Maria G. Delbue, Serena Rossi, Andrea Mazziotti, Romina Borghi, Elisa |
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| Cites_doi | 10.1099/0022-1317-79-4-789 10.3109/13550280009018304 10.1086/321813 10.1128/jcm.32.10.2359-2363.1994 10.1007/BF01322682 10.1007/978-1-4613-2221-4_6 10.1111/j.1469-0691.2004.00882.x 10.1099/0022-1317-82-5-1221 10.1097/00007890-200105150-00020 10.1080/13550280590900382 10.1097/01.MP.0000044622.04245.A9 10.1007/s00705-003-0214-6 10.1002/0471221945.ch7 10.1002/0471221945.ch18 10.5858/2005-129-69-KAUTPI 10.1002/jmv.20474 10.1128/jcm.34.1.159-164.1996 10.1093/infdis/161.6.1128 10.1006/viro.1994.1008 10.1002/0471221945.ch10 10.1080/13550280390241269 10.1016/S1286-4579(00)01339-3 10.1099/0022-1317-80-4-1017 10.1002/jmv.1890470306 |
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| Keywords | Virus Urine cells urinary sediment JC virus Polyomavirus Papovaviridae Sediments JC virus (JCV) Quantitative analysis |
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| References_xml | – reference: Stoner GL, Jobes DV, Cobo MF, Agostini HT, Chima SC, Ryschkewitsch CF. 2000. JC virus as marker of human migration to the Americas. Microbes Infect 2: 1905-1911. – reference: Zheng HJ, Kitamura T, Takasaka T, Chen Q, Yogo Y. 2004. Unambiguous identification of JC polyomavirus strains transmitted from parents to children. Arch Virol 149: 261-273. – reference: Delbue S, Sotgiu G, Fumagalli D, Valli M, Borghi E, Mancuso R, Marchioni E, Maserati R, Ferrante P. 2005b. A case of a PML patient with four different JC virus TCR rearrangements in CSF, blood, serum and urine. J Neurovirol 11: 51-57. – reference: Dörries K, Vogel E, GÜntehr S, Czub S. 1994. Infection of human polyomavirus JC and BK in peripheral blood leukocytes from immunocompetent individuals. Virology 198: 59-70. – reference: Agostini HT, Deckhut A, Jobes DV, Girones R, Schlunck G, Prost MG, Frias C, Perez-Trallero E, Ryschkewitsch CF, Stoner GL. 2001a. Genotypes of JC virus in East, Central and Southwest Europe. J Gen Virol 82: 1221-1231. – reference: Delbue S, Pagani E, Guerini FR, Agliardi C, Mancuso R, Borghi E, Rossi F, Boldorini R, Veggiani C, Car PG, Ferrante P. 2005a. Distribution, characterisation and significance of polyomavirus genomic sequences in tumours of the brain and its covering. J Med Virol 77: 447-454. – reference: Ferrante P, Caldarelli-Stefano R, Omodeo-Zorini E, Boldorini R, Costanzi G. 1995. PCR detection of JC virus DNA in brain tissue from patients with and without progressive multifocal leukoencephalopathy. J Med Virol 47: 219-225. – reference: Vaz B, Cinque P, Pickhardt M, Weber T. 2000. Analysis of the transcriptional control region in progressive multifocal leukoencephalopathy. J Neurovirol 6: 398-409. – reference: Elsner C, Doerries K. 1998. Human polyomavirus JC control region variants in persistenly infected CNS and kidney tissue. J Gen Virol 79: 789-799. – reference: Kitamura T, Aso Y, Kuniyoshi N, Hara K, Yogo Y. 1990. High incidence of urinary JC virus excretion in nonimmunosuppressed older patients. JID 161: 1128-1133. – reference: Agostini HT, Ryschkewitsch CF, Stoner GL. 1996. Genotype profile of human polyomavirus JC excreted in urine of immunocompetent individuals. J Clin Microbiol 34: 159-164. – reference: Polo C, Perez JL, Mielnichuck A, Fedele CG, Niubo J, Tenorio A. 2004. Prevalence and patterns of polyomavirus urinary excretion in immunocompetent adults and children. Clin Microbiol Infect 10: 640-644. – reference: Ciappi S, Azzi A, De Santis R, Leoncini F, Sterrantino G, Mazzotta F, Mecocci L. 1999. Archetypal and rearranged sequences of human polyomavirus JC transcription control region in peripheral blood leukocytes and in cerebrospinal fluid. J Gen Virol 80: 1017-1023. – reference: Reploeg MD, Storch GA, Clifford DB. 2001. BK virus: A clinical review. Clin Infect Dis 33: 191-202. – reference: Hou J, Major EO. 2000. Progressive multifocal leukoencephalopathy: JC virus induced demyelination in the immune compromised host. J Neurovirol 6: 98-100. – reference: Pagani E, Delbue S, Mancuso R, Borghi E, Tarantini L, Ferrante P. 2003. Molecular analysis of JC virus genotypes circulating among the Italian healthy population. J Neurovirol 9: 559-566. – reference: Boldorini R, Veggiani C, Barco D, Monga G. 2005. Kidney and urinary tract Polyomavirus infection and distribution. Arch Pathol Lab Med 129: 69-73. – reference: Randhawa P, Baksh F, Aoki N, Tschirhart D, Finkelstein S. 2001. JC virus infection in allograft kidneys: Analysis by polymerase chain reaction and immunohistochemistry. Transpl 71: 1300-1303. – reference: Agostini HT, Brubaker GR, Shao J, Levin A, Ryschkewitsch CF, Blattner WA, Stoner GL. 1995. BK virus and a new type of JC virus excreted by HIV-1 positive patients in rural Tanzania. Arch Virol 140: 1919-1934. – reference: Boldorini R, Omodeo-Zorini E, Nebuloni M, Benigni E, Vago L, Ferri A, Monga G. 2003. Lytic JC Virus infection in the Kidneys of AIDS subjects. Mod Pathol 16: 35-42. – reference: Jensen PN, Major EO. 2001. A classification scheme for human polyomavirus JCV variants based on the nucleotide sequence of the noncoding regulatory region. J Neurovirol 27: 280-287. – reference: Kitamura T, Kunitake T, Guo J, Tominaga T, Kawabe K, Yogo Y. 1994. Transmission of the human polyomavirus JC virus occurs both within the family and outside the family. 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classification scheme for human polyomavirus JCV variants based on the nucleotide sequence of the noncoding regulatory region publication-title: J Neurovirol – volume: 6 start-page: 98 year: 2000 ident: e_1_2_1_15_1 article-title: Progressive multifocal leukoencephalopathy: JC virus induced demyelination in the immune compromised host publication-title: J Neurovirol – ident: e_1_2_1_25_1 doi: 10.1007/978-1-4613-2221-4_6 – ident: e_1_2_1_20_1 doi: 10.1111/j.1469-0691.2004.00882.x – ident: e_1_2_1_4_1 doi: 10.1099/0022-1317-82-5-1221 – ident: e_1_2_1_21_1 doi: 10.1097/00007890-200105150-00020 – ident: e_1_2_1_10_1 doi: 10.1080/13550280590900382 – ident: e_1_2_1_6_1 doi: 10.1097/01.MP.0000044622.04245.A9 – ident: e_1_2_1_27_1 doi: 10.1007/s00705-003-0214-6 – ident: e_1_2_1_26_1 doi: 10.1002/0471221945.ch7 – ident: e_1_2_1_5_1 doi: 10.1002/0471221945.ch18 – volume: 129 start-page: 69 year: 2005 ident: e_1_2_1_7_1 article-title: Kidney and urinary tract Polyomavirus infection and distribution publication-title: Arch Pathol Lab Med doi: 10.5858/2005-129-69-KAUTPI – ident: e_1_2_1_9_1 doi: 10.1002/jmv.20474 – ident: e_1_2_1_3_1 doi: 10.1128/jcm.34.1.159-164.1996 – ident: e_1_2_1_17_1 doi: 10.1093/infdis/161.6.1128 – ident: e_1_2_1_12_1 doi: 10.1006/viro.1994.1008 – ident: e_1_2_1_11_1 doi: 10.1002/0471221945.ch10 – volume: 9 start-page: 559 year: 2003 ident: e_1_2_1_19_1 article-title: Molecular analysis of JC virus genotypes circulating among the Italian healthy population publication-title: J Neurovirol doi: 10.1080/13550280390241269 – ident: e_1_2_1_23_1 doi: 10.1016/S1286-4579(00)01339-3 – ident: e_1_2_1_8_1 doi: 10.1099/0022-1317-80-4-1017 – ident: e_1_2_1_14_1 doi: 10.1002/jmv.1890470306 |
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| Snippet | Human polyomavirus JC (JCV) infects the worldwide population, remains latent in the kidney, and is excreted in the urine. A longitudinal study was performed in... |
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| SubjectTerms | Adult Aged Biological and medical sciences Biomarkers - urine Capsid Proteins - genetics cells DNA, Viral - urine Female Fundamental and applied biological sciences. Psychology Human viral diseases Humans Infectious diseases Italy JC virus JC virus (JCV) JC Virus - classification JC Virus - isolation & purification JC Virus - physiology Male Medical sciences Microbiology Middle Aged Miscellaneous Polyomavirus Polyomavirus Infections - urine Polyomavirus Infections - virology Regulatory Elements, Transcriptional - genetics Tumor Virus Infections - virology urinary sediment urine Viral diseases Virology Virus Activation Virus Shedding |
| Title | Presence, quantitation and characterization of JC virus in the urine of Italian immunocompetent subjects |
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