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Article ; Online: A polyomavirus peptide binds to the capsid VP1 pore and has potent antiviral activity against BK and JC polyomaviruses.

Kane, Joshua R / Fong, Susan / Shaul, Jacob / Frommlet, Alexandra / Frank, Andreas O / Knapp, Mark / Bussiere, Dirksen E / Kim, Peter / Ornelas, Elizabeth / Cuellar, Carlos / Hyrina, Anastasia / Abend, Johanna R / Wartchow, Charles A

eLife

2020 Volume 9

Abstract: In pursuit of therapeutics for human polyomaviruses, we identified a peptide derived from the BK polyomavirus (BKV) minor structural proteins VP2/3 that is a potent inhibitor of BKV infection with no observable cellular toxicity. The thirteen-residue ... ...

Abstract	In pursuit of therapeutics for human polyomaviruses, we identified a peptide derived from the BK polyomavirus (BKV) minor structural proteins VP2/3 that is a potent inhibitor of BKV infection with no observable cellular toxicity. The thirteen-residue peptide binds to major structural protein VP1 with single-digit nanomolar affinity. Alanine-scanning of the peptide identified three key residues, substitution of each of which results in ~1000 fold loss of binding affinity with a concomitant reduction in antiviral activity. Structural studies demonstrate specific binding of the peptide to the pore of pentameric VP1. Cell-based assays demonstrate nanomolar inhibition (EC
MeSH term(s)	Antiviral Agents/chemistry ; Antiviral Agents/metabolism ; Antiviral Agents/pharmacology ; BK Virus/drug effects ; BK Virus/genetics ; BK Virus/metabolism ; Capsid Proteins/chemistry ; Capsid Proteins/genetics ; Capsid Proteins/metabolism ; Cells, Cultured ; HEK293 Cells ; Humans ; JC Virus/drug effects ; Peptides/chemistry ; Peptides/genetics ; Peptides/metabolism ; Protein Binding
Chemical Substances	Antiviral Agents ; Capsid Proteins ; Peptides ; VP1 protein, polyomavirus
Language	English
Publishing date	2020-01-21
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2687154-3
ISSN	2050-084X ; 2050-084X
ISSN (online)	2050-084X
ISSN	2050-084X
DOI	10.7554/eLife.50722
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Transforming growth factor-beta-mediated regulation of BK virus gene expression.

Abend, Johanna R / Imperiale, Michael J

Virology

2008 Volume 378, Issue 1, Page(s) 6–12

Abstract: The increasing prevalence of BK virus (BKV)-associated diseases in immunosuppressed patients has prompted an investigation of the immune response to BKV, especially the role of cytokines in regulating viral replication. We examined the effect of TGF-beta, ...

Abstract	The increasing prevalence of BK virus (BKV)-associated diseases in immunosuppressed patients has prompted an investigation of the immune response to BKV, especially the role of cytokines in regulating viral replication. We examined the effect of TGF-beta, a cytokine that is stimulated by certain immunosuppressive therapies, on BKV gene expression during lytic infection of renal proximal tubule epithelial cells. Viral gene expression, and specifically the activity of the BKV early promoter, is regulated by TGF-beta in a strain-dependent manner. Promoter activity is upregulated in the presence of TGF-beta for the TU strain of BKV, and not for the Dik, Dunlop, or Proto-2 strains. Using site-directed mutagenesis, we have identified a small segment of the TU promoter that is required for stimulation in response to TGF-beta. These results demonstrate that BKV strains can respond differently to cytokine treatment and suggest that TGF-beta may play a role in the reactivation of BKV.
MeSH term(s)	BK Virus/classification ; BK Virus/genetics ; BK Virus/metabolism ; BK Virus/pathogenicity ; Base Sequence ; Cells, Cultured ; Epithelial Cells/virology ; Gene Expression Regulation, Viral ; Humans ; Kidney Tubules, Proximal/cytology ; Kidney Tubules, Proximal/virology ; Molecular Sequence Data ; Promoter Regions, Genetic ; Smad3 Protein/genetics ; Smad3 Protein/metabolism ; Transforming Growth Factor beta/metabolism ; Viral Proteins/genetics ; Viral Proteins/metabolism
Chemical Substances	Smad3 Protein ; Transforming Growth Factor beta ; Viral Proteins
Language	English
Publishing date	2008-06-17
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	200425-2
ISSN	1096-0341 ; 0042-6822
ISSN (online)	1096-0341
ISSN	0042-6822
DOI	10.1016/j.virol.2008.05.009
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Article ; Online: Achieving efficacy in subjects with sustained pegvaliase-neutralizing antibody responses.

Aryal, Madhukar / Lau, Kelly / Boyer, Ryan / Zhou, Huiyu / Abend, Johanna / Gu, Karen / Olbertz, Joy / Gupta, Soumi / Zoog, Stephen / Larimore, Kevin

Molecular genetics and metabolism

2021 Volume 134, Issue 3, Page(s) 235–242

Abstract: Pegvaliase (Palynziq®) is an enzyme substitution therapy using PEGylated recombinant Anabaena variabilis phenylalanine ammonia lyase (PAL) to reduce blood phenylalanine (Phe) levels in adults with phenylketonuria (PKU). In Phase 3 clinical studies, all ... ...

Abstract	Pegvaliase (Palynziq®) is an enzyme substitution therapy using PEGylated recombinant Anabaena variabilis phenylalanine ammonia lyase (PAL) to reduce blood phenylalanine (Phe) levels in adults with phenylketonuria (PKU). In Phase 3 clinical studies, all subjects treated with pegvaliase developed anti-drug antibodies. To specifically evaluate pegvaliase-neutralizing antibodies (NAbs) and assess impact on pegvaliase efficacy, a novel hybrid ligand-binding/tandem mass spectrometry NAb assay was developed. Analysis of Phase 3 study samples revealed that pegvaliase NAb titers developed during early treatment (≤6 months after treatment initiation), and then plateaued and persisted in the majority of subjects during late treatment (>6 months). Subjects with the lowest/undetectable NAb titers had relatively high plasma pegvaliase concentrations and experienced the most rapid decline in blood Phe concentrations at relatively low pegvaliase dose concentrations. In contrast, subjects with higher NAb titers generally had lower plasma pegvaliase concentrations on similar low doses, with little change in blood Phe concentrations. However, with additional time on treatment and individualized dose titration, the majority of subjects achieved substantial and sustained blood Phe reduction, including those with higher NAb titers. Moreover, after maturation of the anti-pegvaliase immune response, NAb titers were stable over time and did not rise in response to dose increases; thus, subjects did not require additional dose increases to maintain reduction in blood Phe.
MeSH term(s)	Adult ; Antibodies, Neutralizing/blood ; Antibodies, Neutralizing/immunology ; Humans ; Phenylalanine/blood ; Phenylalanine Ammonia-Lyase/adverse effects ; Phenylalanine Ammonia-Lyase/blood ; Phenylalanine Ammonia-Lyase/immunology ; Phenylalanine Ammonia-Lyase/therapeutic use ; Phenylketonurias/drug therapy ; Recombinant Proteins/adverse effects ; Recombinant Proteins/blood ; Recombinant Proteins/immunology ; Recombinant Proteins/therapeutic use
Chemical Substances	Antibodies, Neutralizing ; Recombinant Proteins ; Phenylalanine (47E5O17Y3R) ; Phenylalanine Ammonia-Lyase (EC 4.3.1.24) ; pegvaliase (N6UAH27EUV)
Language	English
Publishing date	2021-10-04
Publishing country	United States
Document type	Clinical Trial, Phase III ; Journal Article ; Multicenter Study ; Randomized Controlled Trial ; Research Support, Non-U.S. Gov't
ZDB-ID	1418518-0
ISSN	1096-7206 ; 1096-7192
ISSN (online)	1096-7206
ISSN	1096-7192
DOI	10.1016/j.ymgme.2021.09.006
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Article ; Online: A polyomavirus peptide binds to the capsid VP1 pore and has potent antiviral activity against BK and JC polyomaviruses

Joshua R Kane / Susan Fong / Jacob Shaul / Alexandra Frommlet / Andreas O Frank / Mark Knapp / Dirksen E Bussiere / Peter Kim / Elizabeth Ornelas / Carlos Cuellar / Anastasia Hyrina / Johanna R Abend / Charles A Wartchow

eLife, Vol

2020 Volume 9

Abstract	In pursuit of therapeutics for human polyomaviruses, we identified a peptide derived from the BK polyomavirus (BKV) minor structural proteins VP2/3 that is a potent inhibitor of BKV infection with no observable cellular toxicity. The thirteen-residue peptide binds to major structural protein VP1 with single-digit nanomolar affinity. Alanine-scanning of the peptide identified three key residues, substitution of each of which results in ~1000 fold loss of binding affinity with a concomitant reduction in antiviral activity. Structural studies demonstrate specific binding of the peptide to the pore of pentameric VP1. Cell-based assays demonstrate nanomolar inhibition (EC50) of BKV infection and suggest that the peptide acts early in the viral entry pathway. Homologous peptide exhibits similar binding to JC polyomavirus VP1 and inhibits infection with similar potency to BKV in a model cell line. Lastly, these studies validate targeting the VP1 pore as a novel strategy for the development of anti-polyomavirus agents.
Keywords	BK polyomavirus ; JC polyomavirus ; peptide ; antiviral ; Medicine ; R ; Science ; Q ; Biology (General) ; QH301-705.5
Subject code	570
Language	English
Publishing date	2020-01-01T00:00:00Z
Publisher	eLife Sciences Publications Ltd
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Correlation of BK Virus Neutralizing Serostatus With the Incidence of BK Viremia in Kidney Transplant Recipients.

Abend, Johanna R / Changala, Marguerite / Sathe, Atul / Casey, Fergal / Kistler, Amy / Chandran, Sindhu / Howard, Abigail / Wojciechowski, David

Transplantation

2017 Volume 101, Issue 6, Page(s) 1495–1505

Abstract: ... serostatus of 116 donors (D)-recipient (R) pairs using infectious BKV neutralization assays ... serostatus groups, with the exception of calculated panel-reactive antibody which was lowest in the D+/R ... confidence interval, 1.9-12.7]; P = 0.0008). Furthermore, donor-recipient pairs with D+/R- neutralizing serostatus had ...

Abstract	Background: BK virus (BKV)-associated nephropathy is the second leading cause of graft loss in kidney transplant recipients. Due to the high prevalence of persistent infection with BKV in the general population, it is possible that either the transplant recipient or donor may act as the source of virus resulting in viruria and viremia. Although several studies suggest a correlation between donor-recipient serostatus and the development of BK viremia, specific risk factors for BKV-related complications in the transplant setting remain to be established. Methods: We retrospectively determined the pretransplant BKV neutralizing serostatus of 116 donors (D)-recipient (R) pairs using infectious BKV neutralization assays with representatives from the 4 major viral serotypes. The neutralizing serostatus of donors and recipients was then correlated with the incidence of BK viremia during the first year posttransplantation. Results: There were no significant differences in baseline demographics or transplant data among the 4 neutralizing serostatus groups, with the exception of calculated panel-reactive antibody which was lowest in the D+/R- group. Recipients of kidneys from donors with significant serum neutralizing activity (D+) had elevated risk for BK viremia, regardless of recipient serostatus (D+ versus D-: odd ratio, 5.0; 95% confidence interval, 1.9-12.7]; P = 0.0008). Furthermore, donor-recipient pairs with D+/R- neutralizing serostatus had the greatest risk for BK viremia (odds ratio, 4.9; 95% confidence interval, 1.7-14.6; P = 0.004). Conclusions: Donor neutralizing serostatus correlates significantly with incidence of posttransplant BK viremia. Determination of donor-recipient neutralizing serostatus may be useful in assessing the risk of BKV infection in kidney transplant recipients.
MeSH term(s)	Adult ; Aged ; Antibodies, Neutralizing/blood ; Antibodies, Viral/blood ; BK Virus/immunology ; Biomarkers/blood ; Chi-Square Distribution ; Enzyme-Linked Immunosorbent Assay ; Female ; Humans ; Immunocompromised Host ; Immunosuppressive Agents/adverse effects ; Incidence ; Kidney Transplantation/adverse effects ; Logistic Models ; Male ; Middle Aged ; Neutralization Tests ; Odds Ratio ; Opportunistic Infections/diagnosis ; Opportunistic Infections/epidemiology ; Opportunistic Infections/immunology ; Opportunistic Infections/virology ; Polyomavirus Infections/diagnosis ; Polyomavirus Infections/epidemiology ; Polyomavirus Infections/immunology ; Polyomavirus Infections/virology ; Retrospective Studies ; Risk Factors ; San Francisco/epidemiology ; Time Factors ; Treatment Outcome ; Tumor Virus Infections/diagnosis ; Tumor Virus Infections/epidemiology ; Tumor Virus Infections/immunology ; Tumor Virus Infections/virology
Chemical Substances	Antibodies, Neutralizing ; Antibodies, Viral ; Biomarkers ; Immunosuppressive Agents
Language	English
Publishing date	2017-06
Publishing country	United States
Document type	Journal Article
ZDB-ID	208424-7
ISSN	1534-6080 ; 0041-1337
ISSN (online)	1534-6080
ISSN	0041-1337
DOI	10.1097/TP.0000000000001261
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Zs.A 488: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Regulation of tumor necrosis factor-like weak inducer of apoptosis receptor protein (TWEAKR) expression by Kaposi's sarcoma-associated herpesvirus microRNA prevents TWEAK-induced apoptosis and inflammatory cytokine expression.

Abend, Johanna R / Uldrick, Thomas / Ziegelbauer, Joseph M

Journal of virology

2010 Volume 84, Issue 23, Page(s) 12139–12151

Abstract: Kaposi's sarcoma (KS)-associated herpesvirus (KSHV) is the causative agent of KS, the second most common AIDS-associated malignancy. KSHV expresses at least 18 different mature microRNAs (miRNAs) during latency. To identify cellular targets of KSHV ... ...

Abstract	Kaposi's sarcoma (KS)-associated herpesvirus (KSHV) is the causative agent of KS, the second most common AIDS-associated malignancy. KSHV expresses at least 18 different mature microRNAs (miRNAs) during latency. To identify cellular targets of KSHV miRNAs, we have analyzed a previously reported series of microarrays examining changes in cellular gene expression in the presence of KSHV miRNAs. Tumor necrosis factor (TNF)-like weak inducer of apoptosis (TWEAK) receptor (TWEAKR) was among the most consistently and robustly downregulated genes in the presence of KSHV miR-K12-10a (miR-K10a). Results from luciferase assays with reporter plasmids containing the 3' untranslated region (UTR) of TWEAKR suggest a targeting of TWEAKR by miR-K10a. The mutation of two predicted miR-K10a recognition sites within the 3' UTR of TWEAKR completely disrupts inhibition by miR-K10a. The expression of TWEAKR was downregulated in cells transfected with miR-K10a as well as during de novo KSHV infection. In a KS tumor-derived endothelial cell line, the downregulation of TWEAKR by miR-K10a resulted in reduced levels of TWEAK-induced caspase activation. In addition, cells transfected with miR-K10a showed less induction of apoptosis by annexin V staining and terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling (TUNEL) assays. Finally, the downregulation of TWEAKR by miR-K10a in primary human endothelial cells resulted in a decrease in levels of expression of the proinflammatory cytokines interleukin-8 (IL-8) and monocyte chemoattractant protein 1 (MCP-1) in response to TWEAK. These results identify and validate an important cellular target of KSHV miRNAs. Furthermore, we demonstrate that a viral miRNA protects cells from apoptosis and suppresses a proinflammatory response, which may have significant implications in the complex context of KS lesions.
MeSH term(s)	Annexin A5 ; Apoptosis/physiology ; Blotting, Western ; Caspases/metabolism ; Cell Line ; Chemokine CCL2/metabolism ; Cytokine TWEAK ; DNA Primers/genetics ; Gene Expression Regulation/physiology ; Herpesvirus 8, Human/genetics ; Humans ; In Situ Nick-End Labeling ; Interleukin-8/metabolism ; Luciferases ; MicroRNAs/genetics ; MicroRNAs/physiology ; Mutagenesis ; Receptors, Tumor Necrosis Factor/genetics ; Receptors, Tumor Necrosis Factor/metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; TWEAK Receptor ; Tumor Necrosis Factors/physiology
Chemical Substances	Annexin A5 ; CCL2 protein, human ; Chemokine CCL2 ; Cytokine TWEAK ; DNA Primers ; Interleukin-8 ; MicroRNAs ; Receptors, Tumor Necrosis Factor ; TNFSF12 protein, human ; TWEAK Receptor ; Tumor Necrosis Factors ; Luciferases (EC 1.13.12.-) ; Caspases (EC 3.4.22.-)
Language	English
Publishing date	2010-09-15
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Intramural
ZDB-ID	80174-4
ISSN	1098-5514 ; 0022-538X
ISSN (online)	1098-5514
ISSN	0022-538X
DOI	10.1128/JVI.00884-10
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Article ; Online: BK virus and human cancer: innocent until proven guilty.

Abend, Johanna R / Jiang, Mengxi / Imperiale, Michael J

Seminars in cancer biology

2009 Volume 19, Issue 4, Page(s) 252–260

Abstract: BK virus (BKV) is a polyomavirus that ubiquitously infects the human population. Following a typically subclinical primary infection, BKV establishes a life-long persistent infection in the kidney and urinary tract. BKV is known to reactivate and cause ... ...

Abstract	BK virus (BKV) is a polyomavirus that ubiquitously infects the human population. Following a typically subclinical primary infection, BKV establishes a life-long persistent infection in the kidney and urinary tract. BKV is known to reactivate and cause severe disease in immunosuppressed patients, particularly renal and bone marrow transplant patients. Infection of BKV in rodent animal models or cells in culture often results in tumor formation or transformation, respectively. When co-expressed with activated oncogenes, BKV large tumor antigen drives the transformation of primary human cells. An etiological role of BKV in human cancer, however, remains controversial. Multiple reports have demonstrated conflicting results in regards to the presence of BKV sequences and/or proteins in various tumor types. This review compiles the most recent findings of BKV detection in a number of human cancers. Due to the lack of conclusive causality data from these studies, there does not appear to be a definitive association between BKV and human cancers.
MeSH term(s)	Animals ; BK Virus/physiology ; Humans ; Neoplasms/virology ; Polyomavirus Infections/complications ; Tumor Virus Infections/complications
Language	English
Publishing date	2009-02-21
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1033980-2
ISSN	1096-3650 ; 1044-579X
ISSN (online)	1096-3650
ISSN	1044-579X
DOI	10.1016/j.semcancer.2009.02.004
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Article ; Online: Global effects of BKV infection on gene expression in human primary kidney epithelial cells.

Abend, Johanna R / Low, Jonathan A / Imperiale, Michael J

Virology

2009 Volume 397, Issue 1, Page(s) 73–79

Abstract: BK virus (BKV) is a ubiquitous human pathogen that establishes a lifelong persistent infection in kidney epithelial cells. BKV reactivation within these cells results in a lytic infection in immunocompromised patients. Little is known about the specific ... ...

Abstract	BK virus (BKV) is a ubiquitous human pathogen that establishes a lifelong persistent infection in kidney epithelial cells. BKV reactivation within these cells results in a lytic infection in immunocompromised patients. Little is known about the specific interactions of BKV and the host cell during persistence and reactivation. We performed global cellular gene expression analyses using microarrays to characterize the global effect of BKV on primary kidney epithelial cells during the viral life cycle. Our results demonstrate that BKV primarily activates genes involved in cell cycle regulation and apoptosis (58% and 44% of upregulated genes at 48 and 72 h post-infection, respectively). Surprisingly, we observed that only four genes were downregulated during infection and that only two genes directly involved in the inflammatory response were differentially expressed. These results provide information about how BKV interacts with a cell type in which it both establishes persistence and undergoes lytic reactivation.
MeSH term(s)	BK Virus/physiology ; Cells, Cultured ; Down-Regulation ; Epithelial Cells/virology ; Gene Expression Profiling ; Host-Pathogen Interactions ; Humans ; Kidney/virology ; Oligonucleotide Array Sequence Analysis ; Protein Biosynthesis ; Up-Regulation ; Virus Activation ; Virus Latency
Language	English
Publishing date	2009-11-28
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	200425-2
ISSN	1096-0341 ; 0042-6822
ISSN (online)	1096-0341
ISSN	0042-6822
DOI	10.1016/j.virol.2009.10.047
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Article: Inhibitory effect of gamma interferon on BK virus gene expression and replication.

Abend, Johanna R / Low, Jonathan A / Imperiale, Michael J

Journal of virology

2007 Volume 81, Issue 1, Page(s) 272–279

Abstract: BK virus (BKV) is widely accepted to be the causative agent of polyomavirus nephropathy. In immunocompromised individuals, especially kidney transplant recipients, BKV can replicate in kidney epithelial cells, causing loss of renal function and eventual ... ...

Abstract	BK virus (BKV) is widely accepted to be the causative agent of polyomavirus nephropathy. In immunocompromised individuals, especially kidney transplant recipients, BKV can replicate in kidney epithelial cells, causing loss of renal function and eventual destruction of the graft. Advances in immunosuppressive therapies may be partially responsible for the increasing incidence of polyomavirus nephropathy among transplant recipients by more effectively eliminating components of the immune system, such as gamma interferon (IFN-gamma)-producing lymphocytes, that keep BKV infections at a subclinical level. In this study, we investigated the role of IFN-gamma in regulating lytic infection by BKV. Treatment with IFN-gamma inhibited the expression of the viral early protein large tumor antigen (TAg) and the late protein VP1 in a dose-dependent manner. We detected 1.6- and 12-fold reductions in TAg transcripts at 48 and 96 h postinfection, respectively, with 250 U/ml IFN-gamma, suggesting that IFN-gamma-mediated inhibition occurs at the level of transcription. Furthermore, IFN-gamma inhibited the level of viral progeny production as much as 50-fold at a multiplicity of infection (MOI) of 0.5 and 80-fold at an MOI of 0.1. The inhibitory effects of IFN-gamma were similar for three different strains of BKV examined. These results indicate an important role for IFN-gamma in regulating BKV lytic infection.
MeSH term(s)	Antiviral Agents/pharmacology ; BK Virus/drug effects ; BK Virus/genetics ; BK Virus/physiology ; Cells, Cultured ; Gene Expression Regulation, Viral/drug effects ; Humans ; Interferon-gamma/pharmacology ; Kinetics ; RNA, Viral/metabolism ; Viral Proteins/antagonists & inhibitors ; Viral Proteins/genetics ; Viral Proteins/metabolism ; Virus Replication/drug effects
Chemical Substances	Antiviral Agents ; RNA, Viral ; Viral Proteins ; Interferon-gamma (82115-62-6)
Language	English
Publishing date	2007-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	80174-4
ISSN	1098-5514 ; 0022-538X
ISSN (online)	1098-5514
ISSN	0022-538X
DOI	10.1128/JVI.01571-06
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Article ; Online: The role of polyomaviruses in human disease.

Jiang, Mengxi / Abend, Johanna R / Johnson, Silas F / Imperiale, Michael J

Virology

2008 Volume 384, Issue 2, Page(s) 266–273

Abstract: The human polyomaviruses, BK virus and JC virus, have long been associated with serious diseases including polyomavirus nephropathy and progressive multifocal leukoencephalopathy. Both viruses establish ubiquitous, persistent infections in healthy ... ...

Abstract	The human polyomaviruses, BK virus and JC virus, have long been associated with serious diseases including polyomavirus nephropathy and progressive multifocal leukoencephalopathy. Both viruses establish ubiquitous, persistent infections in healthy individuals. Reactivation can occur when the immune system is impaired, leading to disease progression. Recently, the human polyomavirus family has expanded with the identification of three new viruses (KI, WU and Merkel cell polyomavirus), all of which may prove to be involved in human disease. This review describes the general aspects of human polyomavirus infections and pathogenicity. Current topics of investigation and future directions in the field are also discussed.
MeSH term(s)	BK Virus/pathogenicity ; Humans ; JC Virus/pathogenicity ; Kidney Diseases/virology ; Leukoencephalopathy, Progressive Multifocal/virology ; Multiple Sclerosis/virology ; Neoplasms/virology ; Polyomavirus/classification ; Polyomavirus/pathogenicity ; Polyomavirus Infections/transmission ; Polyomavirus Infections/virology ; Tumor Virus Infections/virology
Language	English
Publishing date	2008-11-07
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	200425-2
ISSN	1096-0341 ; 0042-6822
ISSN (online)	1096-0341
ISSN	0042-6822
DOI	10.1016/j.virol.2008.09.027
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