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Article: Generation of recombinant influenza A virus without M2 ion-channel protein by introduction of a point mutation at the 5′ end of the viral intron
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TitleGeneration of recombinant influenza A virus without M2 ion-channel protein by introduction of a point mutation at the 5′ end of the viral intron
 
AuthorsCheung, TKW1
Guan, Y1
Ng, SSF1
Chen, H1
Wong, CHK1
Peiris, JSM1
Poon, LLM1
 
Issue Date2005
 
PublisherSociety for General Microbiology. The Journal's web site is located at http://vir.sgmjournals.org
 
CitationJournal Of General Virology, 2005, v. 86 n. 5, p. 1447-1454 [How to Cite?]
DOI: http://dx.doi.org/10.1099/vir.0.80727-0
 
AbstractThe aim of this study was to inhibit influenza virus M2 protein expression by mutating the splicing signal of the M gene. Mutations were introduced into the GU dinucleotide sequence at the 5′-proximal splicing site of the M gene (corresponding to nt 52-53 of M cRNA). Transfected cells expressing mutated M viral ribonucleoproteins failed to generate M2 mRNA. Interestingly, recombinant viruses with mutations at the dinucleotide sequence were viable, albeit attenuated, in cell culture. These recombinants failed to express M2 mRNA and M2 protein. These observations demonstrated that the GU invariant dinucleotide sequence at the 5′-proximal splicing site of M gene is essential for M2 mRNA synthesis. These results also indicated that the M2 ion-channel protein is critical, but not essential, for virus replication in cell culture. This approach may provide a new way of producing attenuated influenza A virus. © 2005 SGM.
 
ISSN0022-1317
2013 Impact Factor: 3.529
 
DOIhttp://dx.doi.org/10.1099/vir.0.80727-0
 
ISI Accession Number IDWOS:000228717200024
 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorCheung, TKW
 
dc.contributor.authorGuan, Y
 
dc.contributor.authorNg, SSF
 
dc.contributor.authorChen, H
 
dc.contributor.authorWong, CHK
 
dc.contributor.authorPeiris, JSM
 
dc.contributor.authorPoon, LLM
 
dc.date.accessioned2008-05-22T04:19:43Z
 
dc.date.available2008-05-22T04:19:43Z
 
dc.date.issued2005
 
dc.description.abstractThe aim of this study was to inhibit influenza virus M2 protein expression by mutating the splicing signal of the M gene. Mutations were introduced into the GU dinucleotide sequence at the 5′-proximal splicing site of the M gene (corresponding to nt 52-53 of M cRNA). Transfected cells expressing mutated M viral ribonucleoproteins failed to generate M2 mRNA. Interestingly, recombinant viruses with mutations at the dinucleotide sequence were viable, albeit attenuated, in cell culture. These recombinants failed to express M2 mRNA and M2 protein. These observations demonstrated that the GU invariant dinucleotide sequence at the 5′-proximal splicing site of M gene is essential for M2 mRNA synthesis. These results also indicated that the M2 ion-channel protein is critical, but not essential, for virus replication in cell culture. This approach may provide a new way of producing attenuated influenza A virus. © 2005 SGM.
 
dc.description.naturepostprint
 
dc.format.extent322748 bytes
 
dc.format.extent110067 bytes
 
dc.format.mimetypeapplication/pdf
 
dc.format.mimetypeapplication/pdf
 
dc.identifier.citationJournal Of General Virology, 2005, v. 86 n. 5, p. 1447-1454 [How to Cite?]
DOI: http://dx.doi.org/10.1099/vir.0.80727-0
 
dc.identifier.doihttp://dx.doi.org/10.1099/vir.0.80727-0
 
dc.identifier.epage1454
 
dc.identifier.isiWOS:000228717200024
 
dc.identifier.issn0022-1317
2013 Impact Factor: 3.529
 
dc.identifier.issue5
 
dc.identifier.openurl
 
dc.identifier.pmid15831957
 
dc.identifier.scopuseid_2-s2.0-18144385402
 
dc.identifier.spage1447
 
dc.identifier.urihttp://hdl.handle.net/10722/48637
 
dc.identifier.volume86
 
dc.languageeng
 
dc.publisherSociety for General Microbiology. The Journal's web site is located at http://vir.sgmjournals.org
 
dc.publisher.placeUnited Kingdom
 
dc.relation.ispartofJournal of General Virology
 
dc.relation.referencesReferences in Scopus
 
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License
 
dc.subject.meshInfluenza a virus
 
dc.subject.meshChemistry
 
dc.subject.meshGenetics
 
dc.subject.meshPoint mutation
 
dc.subject.meshIntrons
 
dc.titleGeneration of recombinant influenza A virus without M2 ion-channel protein by introduction of a point mutation at the 5′ end of the viral intron
 
dc.typeArticle
 
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Author Affiliations
  1. The University of Hong Kong