The Biology and Molecular Biology of JC Virus

Walker, Duard L.; Frisque, Richard J.

doi:10.1007/978-1-4613-2221-4_6

Cited by 95 publications

(73 citation statements)

References 127 publications

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“…The first of these, antedating the idea of rearrangements from an archetypal structure, distinguished regulatory regions with a single copy of the TATA box or the duplication of this element as observed in the prototype isolate, JCV(Mad-1) (Walker & Frisque, 1986). The other two classifications delineate parts of the archetypal regulatory region which tend to be deleted or duplicated in PML brain.…”

Section: Jc Virus (Jcv) Causes the Central Demyelinating Disease Progmentioning

confidence: 99%

JC virus regulatory region rearrangements and genotypes in progressive multifocal leukoencephalopathy: two independent aspects of virus variation.

Agostini¹,

Ryschkewitsch²,

Singer³

et al. 1997

Journal of General Virology

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The human polyomavirus JC (JCV) has a genome of about 5n1 kb in length. The genome codes for six major proteins : the capsid proteins VP1-3, agnoprotein and the regulatory proteins large and small T antigen (Frisque et al., 1984). Replication is controlled by the viral regulatory region which can exist in two major configurations. In general, urinary strains have a non-rearranged (archetypal) regulatory region of 267 bp (Yogo et al., 1990 ;, whereas strains isolated from brain tissue of patients with progressive multifocal leukoencephalopathy (PML) show rearrangements as a result of deletions and\or duplications from the archetypal form (Ault & Stoner, 1993 ; Iida et al., 1993). Within the regulatory region it is the promoter\enhancer containing area between the origin of replication (ori) and the start of the agnoprotein gene which is altered in PML strains.

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Section: Jc Virus (Jcv) Causes the Central Demyelinating Disease Progmentioning

confidence: 99%

JC virus regulatory region rearrangements and genotypes in progressive multifocal leukoencephalopathy: two independent aspects of virus variation.

Agostini¹,

Ryschkewitsch²,

Singer³

et al. 1997

Journal of General Virology

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“…Approximately 60-80% of the human population produce antibodies to BKV and JCV by the second decade of life, with seroconversion occurring mostly during childhood and earlier for BKV than for JCV (Imperiale and Major, 2007;Knowles, 2006;Major et al, 1992;Walker and Frisque, 1986). Simian virus 40 (SV40), a polyomavirus of macaque origin, was introduced into humans presumably as a result of the widespread use of poliovaccines inadvertently contaminated with this virus Cutrone et al, 2005;Stratton et al, 2003;Vilchez and Butel, 2004).…”

Section: Introductionmentioning

confidence: 99%

Detection of polyomavirus SV40 in tonsils from immunocompetent children

Patel

Vilchez

Killen

et al. 2008

Journal of Clinical Virology

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Background-BK virus (BKV), JC virus (JCV) and simian virus 40 (SV40) are nonenveloped DNA viruses, members of the family Polyomaviridae. BK and JC viruses establish persistent infections in humans, and evidence suggests that SV40 can infect humans, as well. Whether persistence occurs in the lymphoid system is unknown.Methods-Paraffin-embedded tonsils from 220 immunocompetent children (mean age 9.3 years) were examined by polymerase chain reaction (PCR) to detect viral DNA of BKV, JCV, SV40, and Epstein-Barr virus (EBV).Results-Polyomavirus-specific DNA sequences were detected in 8.3% (29/351) of specimens collected from 220 children. Twenty-one (9.5%) children had polyomavirus DNA present in at least one tonsil, with sequences identified as SV40 (n=20) and BKV (n=1). Polyomavirus JCV was not detected. Among patients positive for SV40, 8 of 14 (57%) contained viral DNA in both available tonsils. EBV DNA was detected in 99 (28.2%) samples from 67 (30.5%) patients. Eleven samples (3.1%) from 8 (3.6%) children were positive for both polyomavirus and EBV. SV40-positive children were significantly older than the SV40-negative subjects (P < 0.001). T-antigen expression was detected in an SV40 DNA-positive tonsil by immunohistochemistry.Conclusions-These results suggest that SV40 can infect tonsils, that lymphoid tissue may represent a site for polyomavirus persistence, and that immunohistochemistry is not a useful detection assay when there are very few virus-infected cells in a tissue.

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“…Fax j886 4 3847178. e-mail dch!mercury.csmc.edu.tw 1976 ; Walker & Frisque, 1986 ;White et al, 1992). PML is the result of JCV lytic infection of oligodendrocytes (Walker & Frisque, 1986).…”

Section: Introductionmentioning

confidence: 99%

“…The JCV virion contains three capsid proteins (VP1, VP2 and VP3) and a viral minichromosome (Walker & Frisque, 1986). VP1 is the major capsid protein of JCV, constituting approximately 75 % of the capsid shell protein, while VP2 and VP3 are the minor capsid proteins that make up about 10 % of the capsid proteins (Tooze, 1981).…”

Section: Introductionmentioning

confidence: 99%

The major capsid protein, VP1, of human JC virus expressed in Escherichia coli is able to self-assemble into a capsid-like particle and deliver exogenous DNA into human kidney cells.

Wang

Fung

et al. 1999

Journal of General Virology

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The full-length major capsid protein, VP1, of the human polyomavirus JC virus was cloned and expressed in Escherichia coli. VP1 protein expressed in E. coli self-assembled into capsid-like particles and caused haemagglutination of human O-type red blood cells. Caesium chloride density-gradient centrifugation analysis revealed that the capsid-like particles consisted of virionlike pseudovirion and empty capsid-like pseudocapsid populations. The morphology of pseudovirion and pseudocapsid particles was observed under the electron microscope. The pseudovirions contained DNA and RNA molecules but the pseudocapsids did not contain any nucleic acid, as analysed by DNA extraction. DNA-binding activity of VP1 was also demonstrated by the SouthWestern probing method in vitro. Furthermore, pseudocapsids were able to deliver exogenous DNA into human foetal kidney epithelial cells. These results indicate that recombinant JC virus VP1 is able to self-assemble into capsid-like particles and to package DNA in the absence of the minor capsid proteins, VP2 and VP3. This prokaryotic assembly system may facilitate the investigation of maturation mechanism(s) of polyomaviruses. Furthermore, capsid-like particles of JC virus VP1 generated in E. coli potentially could be used as a human gene transfer vector.

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The Biology and Molecular Biology of JC Virus

Cited by 95 publications

References 127 publications

JC virus regulatory region rearrangements and genotypes in progressive multifocal leukoencephalopathy: two independent aspects of virus variation.

JC virus regulatory region rearrangements and genotypes in progressive multifocal leukoencephalopathy: two independent aspects of virus variation.

Detection of polyomavirus SV40 in tonsils from immunocompetent children

The major capsid protein, VP1, of human JC virus expressed in Escherichia coli is able to self-assemble into a capsid-like particle and deliver exogenous DNA into human kidney cells.

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