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Article: Nuclear factor 90 negatively regulates influenza virus replication by interacting with viral nucleoprotein

TitleNuclear factor 90 negatively regulates influenza virus replication by interacting with viral nucleoprotein
Authors
Issue Date2009
PublisherAmerican Society for Microbiology. The Journal's web site is located at http://jvi.asm.org/
Citation
Journal Of Virology, 2009, v. 83 n. 16, p. 7850-7861 How to Cite?
AbstractInteractions between host factors and the viral replication complex play important roles in host adaptation and regulation of influenza virus replication. A cellular protein, nuclear factor 90 (NF90), was copurified with H5N1 viral nucleoprotein (NP) from human cells in which NP was transiently expressed and identified by matrix-assisted laser desorption ionization-time of flight mass spectrometry analysis. In vitro coimmunoprecipitation of NF90 and NP coexpressed in HEK 293T cells or individually expressed in bacterial and HEK 293T cells, respectively, confirmed a direct interaction between NF90 and NP, independent of other subunits of the ribonucleoprotein complex. This interaction was prevented by a mutation, F412A, in the C-terminal region of the NP, indicating that the C-terminal of NP is required for NF90 binding. RNase V treatment did not prevent coprecipitation of NP and NF90, which demonstrates that the interaction is RNA binding independent. After small interfering RNA knockdown of NF90 expression in A549 and HeLa cells, viral polymerase complex activity and virus replication were significantly increased, suggesting that NF90 negatively affects viral replication. Both NP and NF90 colocalized in the nucleus of virus-infected cells during the early phase of infection, suggesting that the interaction between NF90 and NP is an early event in virus replication. Quantitative reverse transcription-PCR showed that NF90 downregulates both viral genome replication and mRNA transcription in infected cells. These results suggest that NF90 inhibits influenza virus replication during the early phase of infection through direct interaction with viral NP. Copyright © 2009, American Society for Microbiology. All Rights Reserved.
Persistent Identifierhttp://hdl.handle.net/10722/59386
ISSN
2015 Impact Factor: 4.606
2015 SCImago Journal Rankings: 3.347
PubMed Central ID
ISI Accession Number ID
Funding AgencyGrant Number
Research Grants Council of the Hong Kong Special Administrative Region (SAR), China74888/05M
7500/06M
Area of Excellence Scheme of the University Grants CommitteeAoE/M-12/06
National Institutes of HealthHHSN2662007 00005C
Research Fund for the Control of Infectious Diseases of the Health, Welfare and Food Bureau of the Hong Kong SAR
Li Ka Shing Foundation
Funding Information:

This study was supported by the Research Grants Council of the Hong Kong Special Administrative Region (SAR), China (HKU 74888/05M and 7500/06M), the Area of Excellence Scheme of the University Grants Committee (grant AoE/M-12/06), the National Institutes of Health (NIAID contract HHSN2662007 00005C), the Research Fund for the Control of Infectious Diseases of the Health, Welfare and Food Bureau of the Hong Kong SAR, and the Li Ka Shing Foundation.

References
Grants

 

DC FieldValueLanguage
dc.contributor.authorWang, Pen_HK
dc.contributor.authorSong, Wen_HK
dc.contributor.authorMok, BWYen_HK
dc.contributor.authorZhao, Pen_HK
dc.contributor.authorQin, Ken_HK
dc.contributor.authorLai, Aen_HK
dc.contributor.authorSmith, GJDen_HK
dc.contributor.authorZhang, Jen_HK
dc.contributor.authorLin, Ten_HK
dc.contributor.authorGuan, Yen_HK
dc.contributor.authorChen, Hen_HK
dc.date.accessioned2010-05-31T03:49:03Z-
dc.date.available2010-05-31T03:49:03Z-
dc.date.issued2009en_HK
dc.identifier.citationJournal Of Virology, 2009, v. 83 n. 16, p. 7850-7861en_HK
dc.identifier.issn0022-538Xen_HK
dc.identifier.urihttp://hdl.handle.net/10722/59386-
dc.description.abstractInteractions between host factors and the viral replication complex play important roles in host adaptation and regulation of influenza virus replication. A cellular protein, nuclear factor 90 (NF90), was copurified with H5N1 viral nucleoprotein (NP) from human cells in which NP was transiently expressed and identified by matrix-assisted laser desorption ionization-time of flight mass spectrometry analysis. In vitro coimmunoprecipitation of NF90 and NP coexpressed in HEK 293T cells or individually expressed in bacterial and HEK 293T cells, respectively, confirmed a direct interaction between NF90 and NP, independent of other subunits of the ribonucleoprotein complex. This interaction was prevented by a mutation, F412A, in the C-terminal region of the NP, indicating that the C-terminal of NP is required for NF90 binding. RNase V treatment did not prevent coprecipitation of NP and NF90, which demonstrates that the interaction is RNA binding independent. After small interfering RNA knockdown of NF90 expression in A549 and HeLa cells, viral polymerase complex activity and virus replication were significantly increased, suggesting that NF90 negatively affects viral replication. Both NP and NF90 colocalized in the nucleus of virus-infected cells during the early phase of infection, suggesting that the interaction between NF90 and NP is an early event in virus replication. Quantitative reverse transcription-PCR showed that NF90 downregulates both viral genome replication and mRNA transcription in infected cells. These results suggest that NF90 inhibits influenza virus replication during the early phase of infection through direct interaction with viral NP. Copyright © 2009, American Society for Microbiology. All Rights Reserved.en_HK
dc.languageengen_HK
dc.publisherAmerican Society for Microbiology. The Journal's web site is located at http://jvi.asm.org/en_HK
dc.relation.ispartofJournal of Virologyen_HK
dc.rightsJournal of Virology. Copyright © American Society for Microbiology.en_HK
dc.rightsCopyright © American Society for Microbiology, Journal of Virology, 2009, v. 83 n. 16, p. 7850-7861-
dc.subject.meshDown-Regulation-
dc.subject.meshInfluenza A Virus, H5N1 Subtype - genetics - physiology-
dc.subject.meshInfluenza, Human - metabolism - virology-
dc.subject.meshNuclear Factor 90 Proteins - chemistry - genetics - metabolism-
dc.subject.meshNucleoproteins - genetics - metabolism-
dc.titleNuclear factor 90 negatively regulates influenza virus replication by interacting with viral nucleoproteinen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0022-538X&volume=83&spage=7850&epage=61&date=2009&atitle=Nuclear+factor+90,+NF90,+negatively+regulates+influenza+virus+replication+by+interacting+with+viral+nucleoproteinen_HK
dc.identifier.emailSmith, GJD: gjsmith@hkucc1.hku.hken_HK
dc.identifier.emailZhang, J: zhangajx@hkucc.hku.hken_HK
dc.identifier.emailGuan, Y: yguan@hkucc.hku.hken_HK
dc.identifier.emailChen, H: hlchen@hku.hken_HK
dc.identifier.authoritySmith, GJD=rp00444en_HK
dc.identifier.authorityZhang, J=rp00413en_HK
dc.identifier.authorityGuan, Y=rp00397en_HK
dc.identifier.authorityChen, H=rp00383en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1128/JVI.00735-09en_HK
dc.identifier.pmid19494010-
dc.identifier.pmcidPMC2715781-
dc.identifier.scopuseid_2-s2.0-67749127718en_HK
dc.identifier.hkuros160812en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-67749127718&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume83en_HK
dc.identifier.issue16en_HK
dc.identifier.spage7850en_HK
dc.identifier.epage7861en_HK
dc.identifier.eissn1098-5514-
dc.identifier.isiWOS:000268208700006-
dc.publisher.placeUnited Statesen_HK
dc.relation.projectControl of Pandemic and Inter-pandemic Influenza-
dc.identifier.scopusauthoridWang, P=13907209900en_HK
dc.identifier.scopusauthoridSong, W=23490429800en_HK
dc.identifier.scopusauthoridMok, BWY=36786012800en_HK
dc.identifier.scopusauthoridZhao, P=34972423500en_HK
dc.identifier.scopusauthoridQin, K=8512090900en_HK
dc.identifier.scopusauthoridLai, A=36769811700en_HK
dc.identifier.scopusauthoridSmith, GJD=8344015800en_HK
dc.identifier.scopusauthoridZhang, J=12752135600en_HK
dc.identifier.scopusauthoridLin, T=7404860987en_HK
dc.identifier.scopusauthoridGuan, Y=7202924055en_HK
dc.identifier.scopusauthoridChen, H=26643315400en_HK
dc.identifier.citeulike4768934-

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