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dc.contributor.authorJia, Qingmei
dc.contributor.authorHogle, James M.
dc.contributor.authorHashikawa, Tsutomu
dc.contributor.authorNomoto, Akio
dc.date.accessioned2019-10-05T09:47:27Z
dc.date.issued2001
dc.identifier.citationJia, Q., J. M. Hogle, T. Hashikawa, and A. Nomoto. 2001. “Molecular Genetic Analysis of Revertants from a Poliovirus Mutant That Is Specifically Adapted to the Mouse Spinal Cord.” Journal of Virology 75 (23): 11766–72. https://doi.org/10.1128/jvi.75.23.11766-11772.2001.
dc.identifier.issn0022-538X
dc.identifier.issn1070-6321
dc.identifier.issn1098-5514
dc.identifier.urihttp://nrs.harvard.edu/urn-3:HUL.InstRepos:41483198*
dc.description.abstractSA virus, a mutant of the Mahoney strain of type 1 poliovirus (PV1/Mahoney), replicates specifically in the spinal cords of mice and causes paralysis, although the PV1/Mahoney strain does not show any mouse neurovirulence (Q. Jia, S. Ohka, K. Iwasaki, K. Tohyama, and A. Nomoto, J. Virol. 73:6041-6047, 1999). The key mutation site for the mouse neurovirulence of SA was mapped to nucleotide (nt) 928 of the genome (A to G), resulting in the amino acid substitution of Met for lie at residue 62 within the capsid protein VP4 (VP4062). A small-plaque phenotype of SA appears to be indicative of its mouse-neurovirulent phenotype. To identify additional amino acid residues involved in the host range determination of PV, a total of 14 large-plaque (LP) variants were isolated from a single point mutant, Mah/I4062M, that showed the SA phenotype. All the LP variants no longer showed any mouse neurovirulence when delivered via an intraspinal inoculation route. Of these, 11 isolates had a back mutation at nt 928 (G to A) that restored the nucleotide of the PV1/Mahoney type. The reversions of the remaining three isolates (LP8, LP9, and LP14) were mediated by a second site mutation. Molecular genetic analysis involving recombinants between Mah/I4062M and the LP variants revealed that the mere substitution of an amino acid residue at position 107 in VP1 (Val to Leu) (LP9), position 33 in VP2 (Val to lie) (LP14), or position 231 in VP3 (Ile to Thr) (LPS) was sufficient to restore the PV1/Mahoney phenotype. These amino acid residues are located either on the surface or inside of the virus particle. Our results indicate that the mouse neurovirulence of PV is determined by the virion surface structure, which is formed by all four capsid proteins.
dc.language.isoen_US
dc.publisherAmerican Society for Microbiology
dash.licenseLAA
dc.titleMolecular Genetic Analysis of Revertants from a Poliovirus Mutant That Is Specifically Adapted to the Mouse Spinal Cord
dc.typeJournal Article
dc.description.versionVersion of Record
dc.relation.journalJournal of Virology
dash.depositing.authorHogle, James M.::b88a5e6fc972147844be38cdc64c65b7::600
dc.date.available2019-10-05T09:47:27Z
dash.workflow.comments1Science Serial ID 62748
dc.identifier.doi10.1128/JVI.75.23.11766-11772.2001
dash.source.volume75;23
dash.source.page11766


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