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Influenza A/Hong Kong/156/1997(H5N1) virus NS1 gene mutations F103L and M106I both increase IFN antagonism, virulence and cytoplasmic localization but differ in binding to RIG-I and CPSF30

dc.contributor.authorDankar, Samar K
dc.contributor.authorMiranda, Elena
dc.contributor.authorForbes, Nicole E
dc.contributor.authorPelchat, Martin
dc.contributor.authorTavassoli, Ali
dc.contributor.authorSelman, Mohammed
dc.contributor.authorPing, Jihui
dc.contributor.authorJia, Jianjun
dc.contributor.authorBrown, Earl G
dc.date.accessioned2014-10-01T02:49:45Z
dc.date.available2014-10-01T02:49:45Z
dc.date.created2013
dc.date.issued2013
dc.description.abstractThe genetic basis for avian to mammalian host switching in influenza A virus is largely unknown. The human A/HK/156/1997 (H5N1) virus that transmitted from poultry possesses NS1 gene mutations F103L + M106I that are virulence determinants in the mouse model of pneumonia; however their individual roles have not been determined. The emergent A/Shanghai/patient1/2013(H7N9)-like viruses also possess these mutations which may contribute to their virulence and ability to switch species.
dc.identifier.citationDankar et al. Virology Journal 2013, 10:243
dc.identifier.doi10.1186/1743-422X-10-243
dc.identifier.urihttp://www.virologyj.com/content/10/1/243
dc.identifier.urihttp://hdl.handle.net/10393/31675
dc.language.isoen
dc.titleInfluenza A/Hong Kong/156/1997(H5N1) virus NS1 gene mutations F103L and M106I both increase IFN antagonism, virulence and cytoplasmic localization but differ in binding to RIG-I and CPSF30
dc.typeArticle

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