Genetics of Picornaviruses

Cooper, Penny

doi:10.1007/978-1-4684-2718-9_4

Cited by 46 publications

(46 citation statements)

References 199 publications

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“…This shift was evident at 2 h postinfection and was complete by 3 h in a wild-type infection. In mutant-infected cells, however, there was a global inhibition of protein synthesis which began at 2 h and became very marked by 4 h postinfection (Fig. 6, lanes 5, 8, and 11), during a period when virus-specific translation was at its height in wild-typeinfected cells.…”

Section: Resultsmentioning

confidence: 96%

Poliovirus mutant that does not selectively inhibit host cell protein synthesis.

Bernstein¹,

Sonenberg²,

Baltimore³

1985

Mol. Cell. Biol.

169

141

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A poliovirus type I (Mahoney strain) mutant was obtained by inserting three base pairs into an infectious cDNA clone. The extra amino acid encoded by the insertion was in the amino-terminal (protein 8) portion of the P2 segment of the polyprotein. The mutant virus makes small plaques on HeLa and monkey kidney (CV-1) cells at all temperatures. It lost the ability to mediate the selective inhibition of host cell translation which ordinarily occurs in the first few hours after infection. As an apparent consequence, the mutant synthesizes far less protein than does wild-type virus. In mutant-infected CV-1 cells enough protein was produced to permit a normal course of RNA replication, but the yield of progeny virus was very low. In mutant-infected HeLa cells there was a premature cessation of both cellular and viral protein synthesis followed by a premature halt of viral RNA synthesis. This nonspecific translational inhibition was distinguishable from wild-type-mediated inhibition and did not appear to be part of an interferon or heat shock response. Because the mutant is recessive, our results imply that (at least in HeLa cells) wild-type poliovirus not only actively inhibits translation of cellular mRNAs, but also avoids early inhibition of its own protein synthesis. Cleavage of the cap-binding complex protein P220, which has been associated with the selective inhibition of capped mRNA translation, did not occur in mutant-infected cells. This result supports the hypothesis that cleavage of P220 plays an important role in normal poliovirus-mediated translational inhibition.It has long been recognized that infection of cells with poliovirus results in a selective inhibition of host cell protein synthesis (for a review, see reference 2). Translation of cellular mRNA steadily declines as virus-specific translation increases; by 2 to 3 h after infection viral RNA, which unlike most other translated eucaryotic RNAs lacks a 5' m7Gp-ppN(m) cap structure (8,28), is translated almost exclusively. Presumably, a viral product mediates this inhibition, but it has not been identified.Results of early studies have shown that translation of cellular mRNA is blocked at the initiation step (19). More specifically, the defective initiation factor appears to be a salt-stable complex composed of a cap-binding protein (CBP) and associated proteins. This complex is thought to be crucial for the attachment of capped mRNAs to 40S ribosomal subunits (for a review, see reference 37). Infected cell extracts do not support the translation of capped RNAs (7,34) or their attachment to the CBP complex (16), but both activities can be restored by the addition of CBP complex from uninfected cells (17, 41). In vivo, the decline in host protein synthesis is preceded by specific cleavage of a 220,000-dalton protein (P220) which is part of the CBP complex (6). It has been proposed that the complex is inactivated by this cleavage (6). A viral product is thought to carry out or promote the cleavage of P220, but the known viral protease (protein 7c) is pr...

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Section: Resultsmentioning

confidence: 96%

Poliovirus mutant that does not selectively inhibit host cell protein synthesis.

Bernstein¹,

Sonenberg²,

Baltimore³

1985

Mol. Cell. Biol.

169

141

View full text Add to dashboard Cite

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“…Recombination is generally believed to occur by a replicative template switch (copy-choice) mode, whereby an RNA molecule initiated by the viral RNA polymerase on one viral RNA template is finished by copying another viral RNA template (Cooper 1977;Kirkegaard and Baltimore 1986;Romanova et al 1986;Arnold and Cameron 1999;Nagy et al 1999;Dzianott et al 2001;Kim and Kao 2001). Similar mechanisms are thought to underlie other covalent viral RNA rearrangements, such as deletions and insertions (duplications).…”

Section: Replicative and Nonreplicative Recombination In Rna Virusesmentioning

confidence: 99%

Nonreplicative homologous RNA recombination: Promiscuous joining of RNA pieces?

Gmyl¹,

Korshenko²,

Belousov³

et al. 2003

RNA

104

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Biologically important joining of RNA pieces in cells, as exemplified by splicing and some classes of RNA editing, is posttranscriptional, whereas in RNA viruses it is generally believed to occur during viral RNA polymerase-dependent RNA synthesis. Here, we demonstrate the assembly of precise genome of an RNA virus (poliovirus) from its cotransfected fragments, which does not require specific RNA sequences, takes place before generation of the viral RNA polymerase, and occurs in different ways: Apparently unrestricted ligation of the terminal nucleotides, joining of any one of the two entire fragments with the relevant internal nucleotide of its partner, or internal crossovers within the overlapping sequence. Incorporation of the entire 5 or 3 partners into the recombinant RNA is activated by the presence of terminal 3-phosphate and 5-OH, respectively. Such postreplicative reactions, fundamentally differing from the known site-specific and structurally demanding cellular RNA rearrangements, might contribute to the origin and evolution of RNA viruses and could generate new RNA species during all stages of biological evolution.

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“…Genetic change in poliovirus can also occur by molecular recombination (Cooper, 1977;Lai, 1992). Genetic recombination of poliovirus vaccine (Sabin) strains has been demonstrated (Kew & Nottay, 1984;Macadam et al, 1989;Lipskaya et al, 1991) and is even frequent (Furione et al, 1993) in strains isolated from vaccine-associated paralytic poliomyelitis cases (VAPP).…”

Section: Maria-magdalena Georgescu* Francis Delpeyroux and Radu Crainicmentioning

confidence: 99%

Tripartite genome organization of a natural type 2 vaccine/nonvaccine recombinant poliovirus

Georgescu

Delpeyroux²,

Crainic³

1995

Journal of General Virology

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Intertypic vaccine/vaccine recombinant polioviruses are frequently isolated from vaccine-associated paralytic poliomyelitis cases (VAPP). We identified a vaccine/ nonvaccine poliovirus recombinant as the causative agent of a lethal VAPP. Partial RNA sequencing revealed a tripartite recombinant structure of the viral genome. This consisted of a central capsid core of vaccine origin flanked by two units of nonvaccine origin. The first nonvaccine genomic unit spanned the whole 5' noncoding region, and the second one almost the entire nonstructural protein-coding region and the 3' noncoding region. Amino acid and nucleotide sequence similarities in the 3' and 5' unidentified regions indicated that the viral donor(s) were poliovirus species, suggesting recombination between a vaccine-derived and a wild poliovirus. The nonvaceine donor(s) could not be identified among the investigated wild polioviruses cocirculating in the same geographical area. This is the first report of a natural recombination event occurring in the 5' genomic extremity of poliovirus. The neurovirulence for transgenic mice and the pathogenicity for humans of the recombinant suggested that the modular genomic organization of this virus might have conferred a selective advantage over its vaccine parent.

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Genetics of Picornaviruses

Cited by 46 publications

References 199 publications

Poliovirus mutant that does not selectively inhibit host cell protein synthesis.

Poliovirus mutant that does not selectively inhibit host cell protein synthesis.

Nonreplicative homologous RNA recombination: Promiscuous joining of RNA pieces?

Tripartite genome organization of a natural type 2 vaccine/nonvaccine recombinant poliovirus

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