Trono, Didier and Andino, Raul and Baltimore, David (1988) An RNA sequence of hundreds of nucleotides at the 5' end of poliovirus RNA is involved in allowing viral protein synthesis. Journal of Virology, 62 (7). pp. 2291-2299. ISSN 0022-538X http://resolver.caltech.edu/CaltechAUTHORS:TROjvir88
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Twenty-one mutations were engineered in the 5' noncoding region of poliovirus type 1 RNA, using an infectious cDNA copy of the viral genome. RNA was made from these constructs and used to transfect HeLa cells. Viable virus was recovered from 12 of these transfection experiments, including six strains with a recognizable phenotype, mapping in four different regions. One mutant of each site was studied in more detail. Mutant 5NC-11, having a 4-base insertion at nucleotide 70, was dramatically deficient in RNA synthesis, suggesting that the far 5' end of the genome is primarily involved in one or more steps of RNA replication. Mutants 5NC-13, 5NC-114, and 5NC-116, mapping at nucleotides 224, 270, and 392, respectively, showed a similar behavior; they made very little viral protein, they did not inhibit host cell translation, and they synthesized a significant amount of viral RNA, although with some delay compared with wild type. These three mutants were efficiently complemented by all other poliovirus mutants tested, except those with lesions in protein 2A. Our results imply that these three mutants map in a region (region P) primarily involved in viral protein synthesis and that their inability to shut off host cell translation is secondary to a quantitative defect in protein 2A. The exact function of region P is still to be determined, but our data supports the hypothesis of a single functional module allowing viral protein synthesis and extending over several hundred nucleotides.
|Additional Information:||Copyright © 1988 by the American Society for Microbiology. Received 28 December 1987/Accepted 1 April 1988 We are grateful to V. R. Racaniello for mutant R2-2A-2, to J. P. Li for mutant 1C-41, and to I. Edery for anti-p220 antiserum. This work was supported by Public Health Service grant AI 22346 to D. B. from the National Institutes of Health. D.T. is the recipient of a Fellowship from the Fondation Suisse de Bourses en Medecine et Biologie. R.A. is the recipient of a Fellowship from the Consejo Nacional de Investigaciones en Ciencia y Tecnica-Argentina.|
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