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Article: Mx1 gene protects mice against the highly lethal human H5N1 influenza virus
Title | Mx1 gene protects mice against the highly lethal human H5N1 influenza virus |
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Authors | |
Keywords | H5N1 Influenza Mx1 Polymerase Protection |
Issue Date | 2007 |
Publisher | Landes Bioscience. The Journal's web site is located at http://www.landesbioscience.com/journals/cc |
Citation | Cell Cycle, 2007, v. 6 n. 19, p. 2417-2421 How to Cite? |
Abstract | We investigated the importance of the host Mx1 gene in protection against highly pathogenic H5N1 avian influenza virus. Mice expressing the Mx1 gene survived infection with the lethal human H5N1 isolate A/Vietnam/1203/04 and with reassortants combining its genes with those of the non-lethal virus A/chicken/Vietnam/C58/04, while all Mx1-/- mice succumbed. Mx1-expressing mice showed lower organ virus titers, fewer lesions, and less pulmonary inflammation. Our data support the hypothesis that Mx1 expression protects mice against the high pathogenicity of H5N1 virus through inhibition of viral polymerase activity ultimately resulting in reduced viral growth and spread. Drugs that mimic this mechanism may be protective in humans. ©2007 Landes Bioscience. |
Persistent Identifier | http://hdl.handle.net/10722/179804 |
ISSN | 2023 Impact Factor: 3.4 2023 SCImago Journal Rankings: 0.947 |
ISI Accession Number ID | |
References |
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Salomon, R | en_US |
dc.contributor.author | Staeheli, P | en_US |
dc.contributor.author | Kochs, G | en_US |
dc.contributor.author | Yen, HL | en_US |
dc.contributor.author | Franks, J | en_US |
dc.contributor.author | Rehg, JE | en_US |
dc.contributor.author | Webster, RG | en_US |
dc.contributor.author | Hoffmann, E | en_US |
dc.date.accessioned | 2012-12-19T10:04:57Z | - |
dc.date.available | 2012-12-19T10:04:57Z | - |
dc.date.issued | 2007 | en_US |
dc.identifier.citation | Cell Cycle, 2007, v. 6 n. 19, p. 2417-2421 | en_US |
dc.identifier.issn | 1538-4101 | en_US |
dc.identifier.uri | http://hdl.handle.net/10722/179804 | - |
dc.description.abstract | We investigated the importance of the host Mx1 gene in protection against highly pathogenic H5N1 avian influenza virus. Mice expressing the Mx1 gene survived infection with the lethal human H5N1 isolate A/Vietnam/1203/04 and with reassortants combining its genes with those of the non-lethal virus A/chicken/Vietnam/C58/04, while all Mx1-/- mice succumbed. Mx1-expressing mice showed lower organ virus titers, fewer lesions, and less pulmonary inflammation. Our data support the hypothesis that Mx1 expression protects mice against the high pathogenicity of H5N1 virus through inhibition of viral polymerase activity ultimately resulting in reduced viral growth and spread. Drugs that mimic this mechanism may be protective in humans. ©2007 Landes Bioscience. | en_US |
dc.language | eng | en_US |
dc.publisher | Landes Bioscience. The Journal's web site is located at http://www.landesbioscience.com/journals/cc | en_US |
dc.relation.ispartof | Cell Cycle | en_US |
dc.subject | H5N1 | - |
dc.subject | Influenza | - |
dc.subject | Mx1 | - |
dc.subject | Polymerase | - |
dc.subject | Protection | - |
dc.subject.mesh | Animals | en_US |
dc.subject.mesh | Chickens | en_US |
dc.subject.mesh | Gtp-Binding Proteins - Genetics - Immunology | en_US |
dc.subject.mesh | Humans | en_US |
dc.subject.mesh | Influenza A Virus, H5n1 Subtype - Metabolism | en_US |
dc.subject.mesh | Influenza, Human - Immunology - Virology | en_US |
dc.subject.mesh | Liver - Cytology - Metabolism | en_US |
dc.subject.mesh | Lung - Cytology - Metabolism | en_US |
dc.subject.mesh | Mice | en_US |
dc.subject.mesh | Mice, Inbred Strains | en_US |
dc.subject.mesh | Orthomyxoviridae Infections - Immunology - Virology | en_US |
dc.subject.mesh | Viral Proteins - Metabolism | en_US |
dc.title | Mx1 gene protects mice against the highly lethal human H5N1 influenza virus | en_US |
dc.type | Article | en_US |
dc.identifier.email | Yen, HL: hyen@hku.hk | en_US |
dc.identifier.authority | Yen, HL=rp00304 | en_US |
dc.description.nature | link_to_subscribed_fulltext | en_US |
dc.identifier.doi | 10.4161/cc.6.19.4779 | - |
dc.identifier.pmid | 17700072 | - |
dc.identifier.scopus | eid_2-s2.0-35848938278 | en_US |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-35848938278&selection=ref&src=s&origin=recordpage | en_US |
dc.identifier.volume | 6 | en_US |
dc.identifier.issue | 19 | en_US |
dc.identifier.spage | 2417 | en_US |
dc.identifier.epage | 2421 | en_US |
dc.identifier.isi | WOS:000251085700018 | - |
dc.publisher.place | United States | en_US |
dc.identifier.scopusauthorid | Salomon, R=12786463900 | en_US |
dc.identifier.scopusauthorid | Staeheli, P=7004400156 | en_US |
dc.identifier.scopusauthorid | Kochs, G=7003794464 | en_US |
dc.identifier.scopusauthorid | Yen, HL=7102476668 | en_US |
dc.identifier.scopusauthorid | Franks, J=12786180500 | en_US |
dc.identifier.scopusauthorid | Rehg, JE=7004835777 | en_US |
dc.identifier.scopusauthorid | Webster, RG=36048363100 | en_US |
dc.identifier.scopusauthorid | Hoffmann, E=7201369718 | en_US |
dc.identifier.issnl | 1551-4005 | - |