Monoclonal antibody identification of a 100-kDa membrane protein in HeLa cells and human spinal cord involved in poliovirus attachment.

Shepley, Michael P.; Sherry, Barbara; Weiner, Howard L.

doi:10.1073/pnas.85.20.7743

Cited by 43 publications

(40 citation statements)

References 25 publications

(21 reference statements)

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“…Some of our results showed that poliovirus replication in human endothelial cells might be involved in poliovirus transport across the blood-brain barrier (Couderc et aL, 1989b). The study of poliomyelitis pathogenesis will be benefited by using knowledge acquired from new data emerging from molecular characterization of the cellular poliovirus receptor (Shepley et al, 1988;Mendelsohn et al, 1989). Molecular probes which detect poliovirus receptor transcripts will help define human tissues susceptible to virus infection.…”

Section: Discussionmentioning

confidence: 99%

Molecular Pathogenesis of Neural Lesions Induced by Poliovirus Type 1

Couderc

Christodoulou

Kopecká

et al. 1989

Journal of General Virology

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SUMMARYUsing in situ hybridization techniques for viral RNA and employing a specific riboprobe, we have detected virus in neural cells of monkeys infected with poliovirus type l (PV-1) by the intraspinal route. In monkeys paralysed after inoculation of a neurovirulent revertant of PV-1/Sabin strain, viral RNA was detected in motor neurons and their processes, and in polymorphonuclear and small neural cells. Quantitative in situ hybridization provided evidence of viral replication in individual cells suggesting that the death of motor neurons was due to the direct effect of poliovirus replication in these cells. The histological study of neural lesions of monkeys paralysed after infection with the attenuated Sabin strain of PV-1 revealed two major differences compared to monkeys infected with a virulent strain: (i) the number of destroyed moto r neurons was reduced and limited to the site of inoculation and (ii) the inflammatory reaction was localized but more intense. An account is given of the difference in histopathology induced by virulent and attenuated strains of PV-1 in the central nervous system.

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Section: Discussionmentioning

confidence: 99%

Molecular Pathogenesis of Neural Lesions Induced by Poliovirus Type 1

Couderc

Christodoulou

Kopecká

et al. 1989

Journal of General Virology

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“…This was repeated until passage 6. Plaque purification of virus was done at 39.5°C similarly to plaque assays except that cells were stained as described by Shepley et al (52). Plaques of different sizes were picked through the agar with disposable tips attached to a micropipettor.…”

Section: Methodsmentioning

confidence: 99%

A Cysteine-Rich Motif in Poliovirus Protein 2C ^ATPase Is Involved in RNA Replication and Binds Zinc In Vitro

Pfister

Jones

Wimmer

2000

J Virol

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Protein 2CATPase of picornaviruses is involved in the rearrangement of host cell organelles, viral RNA replication, and encapsidation. However, the biochemical and molecular mechanisms by which 2C ATPase engages in these processes are not known. To characterize functional domains of 2C ATPase , we have focused on a cysteine-rich motif near the carboxy terminus of poliovirus 2C ATPase . This region, which is well conserved among enteroviruses and rhinoviruses displaying an amino acid arrangement resembling zinc finger motifs, was studied by genetic and biochemical analyses. A mutation that replaced the first cysteine residue of the motif with a serine was lethal. A mutant virus which lacked the second of four potential coordination sites for zinc was temperature sensitive. At the restrictive temperature, RNA replication was inhibited whereas translation and polyprotein processing, assayed in vitro and in vivo, appeared to be normal. An intragenomic second-site revertant which reinserted the missing coordination site for zinc and recovered RNA replication at the restrictive temperature was isolated. The cysteine-rich motif was sufficient to bind zinc in vitro, as assessed in the presence of 4-(2-pyridylazo)resorcinol by a colorimetric assay. Zinc binding, however, was not required for hydrolysis of ATP. 2CATPase as well as its precursors 2BC and P2 were found to exist in a reduced form in poliovirus-infected cells.Picornaviridae is a family of nonenveloped, single-stranded positive-sense RNA viruses. The family is subdivided into six genera: Enterovirus, Rhinovirus, Parechovirus, Cardiovirus, Aphthovirus, and Hepatovirus. The most intensively studied picornavirus is Poliovirus, a member of the genus Enterovirus and the causative agent of poliomyelitis.The mechanism of replication of picornavirus genomes is poorly understood. As the genome enters the host cells, it does not find enzymes specific for RNA-dependent RNA synthesis. Therefore, the genomes of picornaviruses contain sequences that code for several proteins designed to replicate the viral RNA. The genomes of picornaviruses encode one polyprotein that is cleaved by endogenous proteinases into functional proteins (63). The primer-and template-dependent RNA polymerase 3D pol takes a central role in RNA replication. In vitro, the enzyme catalyzes three different types of reactions. First, 3D pol synthesizes its primer by uridylylating the genome-linked protein VPg to VPg-pU(pU) (43) and uses this nucleotidyl protein to initiate chain elongation, a process that has been called protein priming (43,49). Second, 3D pol transcribes the RNA templates, yielding minus-and plus-strand RNA (21, 48). Third, 3D pol unwinds double-stranded RNA during chain elongation (13).Biochemical and genetic evidence indicate that 3D pol is not sufficient for RNA replication and that additional viral (63) and cellular proteins are required (reviewed in reference 65). Little is known about the mechanisms by which accessory proteins participate in RNA replication. Among the virus-encoded...

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“…The cellular receptors have now been isolated for both poliovirus (Mendelsohn et al, 1986(Mendelsohn et al, , 1989Shepley et al, 1988) and the major group rhinoviruses (Greve et al, 1989;Staunton et al, 1989); however, the attachment of HAV has not been characterized extensively (Seganti et al, 1987(Seganti et al, , 1989. Viruses can interact with cells in a variety of ways (Dimmock, 1982;Hsu et al, 1988;Marsh & Helenius, 1989;Reagan et al, 1984); in addition to attaching to specific receptors, it has been shown that viruses can bind by indirect mechanisms, for example the attachment of dengue virus to cells bearing Fc receptors is enhanced by antibody raised to the virus (Halstead & O'Rourke, 1977), whereas cytomegalovirus exploits flz-microglobulin in its interaction with cells (Grundy et al, 1987).…”

Section: Introductionmentioning

confidence: 99%

Parameters influencing the attachment of hepatitis A virus to a variety of continuous cell lines

Zajac

Amphlett²,

Rowlands³

et al. 1991

Journal of General Virology

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We have investigated the interactions of purified radiolabelled hepatitis A virus (HAV) with a variety of continuous cell lines. Virus labelled either in vitro with radiolabelled iodine or in vivo with radiolabelled uridine bound to cells with similar efficiency. Attachment to BS-C-1 cells was calcium ion-dependent and this correlated with infectivity assay results. The cell tropism of HAV attachment was examined using cell suspensions and confluent cell monolayers at both 4 °C and 37 °C. The maximum level of attachment was observed at 4 *C with cells in suspension, but was severely inhibited by 2 % foetal calf serum; these results again correlated with infectivity assays. The components of serum which inhibit attachment have been characterized by gel filtration chromatography, sucrose density gradient analysis, immunoprecipitation and Western blotting. The data show that such components are of high Mr and that the serum glycoprotein, ct2-macroglobulin, can partly mimic the inhibitory effect of whole serum.

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Monoclonal antibody identification of a 100-kDa membrane protein in HeLa cells and human spinal cord involved in poliovirus attachment.

Cited by 43 publications

References 25 publications

Molecular Pathogenesis of Neural Lesions Induced by Poliovirus Type 1

Molecular Pathogenesis of Neural Lesions Induced by Poliovirus Type 1

A Cysteine-Rich Motif in Poliovirus Protein 2C ^ATPase Is Involved in RNA Replication and Binds Zinc In Vitro

Parameters influencing the attachment of hepatitis A virus to a variety of continuous cell lines

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Monoclonal antibody identification of a 100-kDa membrane protein in HeLa cells and human spinal cord involved in poliovirus attachment.

Cited by 43 publications

References 25 publications

Molecular Pathogenesis of Neural Lesions Induced by Poliovirus Type 1

Molecular Pathogenesis of Neural Lesions Induced by Poliovirus Type 1

A Cysteine-Rich Motif in Poliovirus Protein 2C ATPase Is Involved in RNA Replication and Binds Zinc In Vitro

Parameters influencing the attachment of hepatitis A virus to a variety of continuous cell lines

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A Cysteine-Rich Motif in Poliovirus Protein 2C ^ATPase Is Involved in RNA Replication and Binds Zinc In Vitro