Mammalian-adaptive mutation NP-Q357K in Eurasian H1N1 Swine Influenza viruses determines the virulence phenotype in mice
It has recently been proposed that the Eurasian avian-like H1N1 (EA H1N1) swine influenza virus (SIV) is one of the most likely zoonotic viruses to cause the next influenza pandemic. Two main genotypes EA H1N1 viruses have been recognized to be infected humans in China. Our study finds that one of t...
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Taylor & Francis Group
2019-01-01
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| Series: | Emerging Microbes and Infections |
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| Online Access: | https://www.tandfonline.com/doi/10.1080/22221751.2019.1635873 |
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| author | Wenfei Zhu Zhaomin Feng Yongkun Chen Lei Yang Jia Liu Xiyan Li Suli Liu Lijuan Zhou Hejiang Wei Rongbao Gao Dayan Wang Yuelong Shu |
| author_facet | Wenfei Zhu Zhaomin Feng Yongkun Chen Lei Yang Jia Liu Xiyan Li Suli Liu Lijuan Zhou Hejiang Wei Rongbao Gao Dayan Wang Yuelong Shu |
| author_sort | Wenfei Zhu |
| collection | DOAJ |
| description | It has recently been proposed that the Eurasian avian-like H1N1 (EA H1N1) swine influenza virus (SIV) is one of the most likely zoonotic viruses to cause the next influenza pandemic. Two main genotypes EA H1N1 viruses have been recognized to be infected humans in China. Our study finds that one of the genotypes JS1-like viruses are avirulent in mice. However, the other are HuN-like viruses and are virulent in mice. The molecular mechanism underlying this difference shows that the NP gene determines the virulence of the EA H1N1 viruses in mice. In addition, a single substitution, Q357K, in the NP protein of the EA H1N1 viruses alters the virulence phenotype. This substitution is a typical human signature marker, which is prevalent in human viruses but rarely detected in avian influenza viruses. The NP-Q357K substitution is readily to be occurred when avian influenza viruses circulate in pigs, and may facilitate their infection of humans and allow viruses also carrying NP-357K to circulate in humans. Our study demonstrates that the substitution Q357K in the NP protein plays a key role in the virulence phenotype of EA H1N1 SIVs, and provides important information for evaluating the pandemic risk of field influenza strains. |
| format | Article |
| id | doaj-art-aac0513182c64ab4b01b39c5fdff91ea |
| institution | OA Journals |
| issn | 2222-1751 |
| language | English |
| publishDate | 2019-01-01 |
| publisher | Taylor & Francis Group |
| record_format | Article |
| series | Emerging Microbes and Infections |
| spelling | doaj-art-aac0513182c64ab4b01b39c5fdff91ea2025-08-20T02:08:12ZengTaylor & Francis GroupEmerging Microbes and Infections2222-17512019-01-018198999910.1080/22221751.2019.1635873Mammalian-adaptive mutation NP-Q357K in Eurasian H1N1 Swine Influenza viruses determines the virulence phenotype in miceWenfei Zhu0Zhaomin Feng1Yongkun Chen2Lei Yang3Jia Liu4Xiyan Li5Suli Liu6Lijuan Zhou7Hejiang Wei8Rongbao Gao9Dayan Wang10Yuelong Shu11National Institute for Viral Disease Control and Prevention, Collaboration Innovation Center for Diagnosis and Treatment of Infectious Diseases, Chinese Center for Disease Control and Prevention, Beijing, People’s Republic of ChinaNational Institute for Viral Disease Control and Prevention, Collaboration Innovation Center for Diagnosis and Treatment of Infectious Diseases, Chinese Center for Disease Control and Prevention, Beijing, People’s Republic of ChinaSchool of Public Health (Shenzhen), Sun Yat-sen University, Guangdong, People’s Republic of ChinaNational Institute for Viral Disease Control and Prevention, Collaboration Innovation Center for Diagnosis and Treatment of Infectious Diseases, Chinese Center for Disease Control and Prevention, Beijing, People’s Republic of ChinaNational Institute for Viral Disease Control and Prevention, Collaboration Innovation Center for Diagnosis and Treatment of Infectious Diseases, Chinese Center for Disease Control and Prevention, Beijing, People’s Republic of ChinaNational Institute for Viral Disease Control and Prevention, Collaboration Innovation Center for Diagnosis and Treatment of Infectious Diseases, Chinese Center for Disease Control and Prevention, Beijing, People’s Republic of ChinaSchool of Public Health (Shenzhen), Sun Yat-sen University, Guangdong, People’s Republic of ChinaNational Institute for Viral Disease Control and Prevention, Collaboration Innovation Center for Diagnosis and Treatment of Infectious Diseases, Chinese Center for Disease Control and Prevention, Beijing, People’s Republic of ChinaNational Institute for Viral Disease Control and Prevention, Collaboration Innovation Center for Diagnosis and Treatment of Infectious Diseases, Chinese Center for Disease Control and Prevention, Beijing, People’s Republic of ChinaNational Institute for Viral Disease Control and Prevention, Collaboration Innovation Center for Diagnosis and Treatment of Infectious Diseases, Chinese Center for Disease Control and Prevention, Beijing, People’s Republic of ChinaNational Institute for Viral Disease Control and Prevention, Collaboration Innovation Center for Diagnosis and Treatment of Infectious Diseases, Chinese Center for Disease Control and Prevention, Beijing, People’s Republic of ChinaNational Institute for Viral Disease Control and Prevention, Collaboration Innovation Center for Diagnosis and Treatment of Infectious Diseases, Chinese Center for Disease Control and Prevention, Beijing, People’s Republic of ChinaIt has recently been proposed that the Eurasian avian-like H1N1 (EA H1N1) swine influenza virus (SIV) is one of the most likely zoonotic viruses to cause the next influenza pandemic. Two main genotypes EA H1N1 viruses have been recognized to be infected humans in China. Our study finds that one of the genotypes JS1-like viruses are avirulent in mice. However, the other are HuN-like viruses and are virulent in mice. The molecular mechanism underlying this difference shows that the NP gene determines the virulence of the EA H1N1 viruses in mice. In addition, a single substitution, Q357K, in the NP protein of the EA H1N1 viruses alters the virulence phenotype. This substitution is a typical human signature marker, which is prevalent in human viruses but rarely detected in avian influenza viruses. The NP-Q357K substitution is readily to be occurred when avian influenza viruses circulate in pigs, and may facilitate their infection of humans and allow viruses also carrying NP-357K to circulate in humans. Our study demonstrates that the substitution Q357K in the NP protein plays a key role in the virulence phenotype of EA H1N1 SIVs, and provides important information for evaluating the pandemic risk of field influenza strains.https://www.tandfonline.com/doi/10.1080/22221751.2019.1635873Eurasian avian-like H1N1 swine influenza virusesNP geneNP-K357Qpathogenicitypandemic potential |
| spellingShingle | Wenfei Zhu Zhaomin Feng Yongkun Chen Lei Yang Jia Liu Xiyan Li Suli Liu Lijuan Zhou Hejiang Wei Rongbao Gao Dayan Wang Yuelong Shu Mammalian-adaptive mutation NP-Q357K in Eurasian H1N1 Swine Influenza viruses determines the virulence phenotype in mice Emerging Microbes and Infections Eurasian avian-like H1N1 swine influenza viruses NP gene NP-K357Q pathogenicity pandemic potential |
| title | Mammalian-adaptive mutation NP-Q357K in Eurasian H1N1 Swine Influenza viruses determines the virulence phenotype in mice |
| title_full | Mammalian-adaptive mutation NP-Q357K in Eurasian H1N1 Swine Influenza viruses determines the virulence phenotype in mice |
| title_fullStr | Mammalian-adaptive mutation NP-Q357K in Eurasian H1N1 Swine Influenza viruses determines the virulence phenotype in mice |
| title_full_unstemmed | Mammalian-adaptive mutation NP-Q357K in Eurasian H1N1 Swine Influenza viruses determines the virulence phenotype in mice |
| title_short | Mammalian-adaptive mutation NP-Q357K in Eurasian H1N1 Swine Influenza viruses determines the virulence phenotype in mice |
| title_sort | mammalian adaptive mutation np q357k in eurasian h1n1 swine influenza viruses determines the virulence phenotype in mice |
| topic | Eurasian avian-like H1N1 swine influenza viruses NP gene NP-K357Q pathogenicity pandemic potential |
| url | https://www.tandfonline.com/doi/10.1080/22221751.2019.1635873 |
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