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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

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
Authors
Issue Date2005
PublisherSociety for General Microbiology. The Journal's web site is located at http://vir.sgmjournals.org
Citation
Journal Of General Virology, 2005, v. 86 n. 5, p. 1447-1454 How to Cite?
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.
Persistent Identifierhttp://hdl.handle.net/10722/48637
ISSN
2014 Impact Factor: 3.183
2014 SCImago Journal Rankings: 1.457
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorCheung, TKWen_HK
dc.contributor.authorGuan, Yen_HK
dc.contributor.authorNg, SSFen_HK
dc.contributor.authorChen, Hen_HK
dc.contributor.authorWong, CHKen_HK
dc.contributor.authorPeiris, JSMen_HK
dc.contributor.authorPoon, LLMen_HK
dc.date.accessioned2008-05-22T04:19:43Z-
dc.date.available2008-05-22T04:19:43Z-
dc.date.issued2005en_HK
dc.identifier.citationJournal Of General Virology, 2005, v. 86 n. 5, p. 1447-1454en_HK
dc.identifier.issn0022-1317en_HK
dc.identifier.urihttp://hdl.handle.net/10722/48637-
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.en_HK
dc.format.extent322748 bytes-
dc.format.extent110067 bytes-
dc.format.mimetypeapplication/pdf-
dc.format.mimetypeapplication/pdf-
dc.languageengen_HK
dc.publisherSociety for General Microbiology. The Journal's web site is located at http://vir.sgmjournals.orgen_HK
dc.relation.ispartofJournal of General Virologyen_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subject.meshInfluenza a virusen_HK
dc.subject.meshChemistryen_HK
dc.subject.meshGeneticsen_HK
dc.subject.meshPoint mutationen_HK
dc.subject.meshIntronsen_HK
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 intronen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0022-1317&volume=86&issue=5&spage=1447&epage=1454&date=2005&atitle=Generation+of+recombinant+influenza+A+virus+without+M2+ion-channel+protein+by+introduction+of+a+point+mutation+at+the+5+end+of+the+viral+intronen_HK
dc.identifier.emailGuan, Y: yguan@hkucc.hku.hken_HK
dc.identifier.emailChen, H: hlchen@hku.hken_HK
dc.identifier.emailPeiris, JSM: malik@hkucc.hku.hken_HK
dc.identifier.emailPoon, LLM: llmpoon@hkucc.hku.hken_HK
dc.identifier.authorityGuan, Y=rp00397en_HK
dc.identifier.authorityChen, H=rp00383en_HK
dc.identifier.authorityPeiris, JSM=rp00410en_HK
dc.identifier.authorityPoon, LLM=rp00484en_HK
dc.description.naturepostprinten_HK
dc.identifier.doi10.1099/vir.0.80727-0en_HK
dc.identifier.pmid15831957-
dc.identifier.scopuseid_2-s2.0-18144385402en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-18144385402&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume86en_HK
dc.identifier.issue5en_HK
dc.identifier.spage1447en_HK
dc.identifier.epage1454en_HK
dc.identifier.isiWOS:000228717200024-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridCheung, TKW=16229531100en_HK
dc.identifier.scopusauthoridGuan, Y=7202924055en_HK
dc.identifier.scopusauthoridNg, SSF=8602085800en_HK
dc.identifier.scopusauthoridChen, H=26643315400en_HK
dc.identifier.scopusauthoridWong, CHK=11039790300en_HK
dc.identifier.scopusauthoridPeiris, JSM=7005486823en_HK
dc.identifier.scopusauthoridPoon, LLM=7005441747en_HK

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