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

Dankar, Samar KMiranda, ElenaForbes, Nicole EPelchat, MartinTavassoli, AliSelman, MohammedPing, JihuiJia, JianjunBrown, Earl G2014-10-012014-10-0120132013Dankar et al. Virology Journal 2013, 10:243http://www.virologyj.com/content/10/1/243http://hdl.handle.net/10393/31675The 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.enInfluenza 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 CPSF30Article10.1186/1743-422X-10-243