Characterization of H7N9 influenza A viruses isolated from humans
Here, biological attributes of two early human isolates of the newly emerged H7N9 influenza viruses are characterized: the potential of these viruses to infect and/or transmit within various animal models is discussed, as is their relative sensitivity to neuraminidase inhibitors and experimental pol...
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| Published in | Nature (London) Vol. 501; no. 7468; pp. 551 - 555 |
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| Main Authors | , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
London
Nature Publishing Group UK
26.09.2013
Nature Publishing Group |
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| Online Access | Get full text |
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| Abstract | Here, biological attributes of two early human isolates of the newly emerged H7N9 influenza viruses are characterized: the potential of these viruses to infect and/or transmit within various animal models is discussed, as is their relative sensitivity to neuraminidase inhibitors and experimental polymerase inhibitors compared to an H1N1 pandemic strain.
Transmission of emerging H7N9 virus
By 20 July 2013, there had been 134 laboratory-confirmed human cases of infection with avian influenza A H7N9 virus infection, including 43 deaths.
Yoshihiro Kawaoka and colleagues characterize the biology of two recent isolates of the virus. They provide a wealth of data from infections in mice, pigs, macaques and ferrets. H7N9 virus is shown to be less sensitive to neuraminidase inhibitors than pandemic H1N1 virus, but equally susceptible to an experimental polymerase inhibitor. Terrence Tumpey and colleagues determine the capacity of two clinical H7N9 isolates to cause disease and transmit between mammals. They show that the virus can replicate in human airway cells and in the respiratory tract of ferrets to a higher level than can seasonal H3N2 virus, and show higher lethality in mice than genetically related H7N9 and H9N2 viruses. In transmission studies, the H7N9 virus showed limited transmission in ferrets by respiratory droplets. Ron Fouchier and colleagues investigate the transmissibility of H7N9 virus between ferrets. They show that airborne transmission can occur, but inefficiently. They also show that on passage in ferrets, virus variants that have higher avian receptor binding, higher pH of fusion and lower thermostability are selected, and they suggest that these characteristics may result in reduced transmissibility.
Avian influenza A viruses rarely infect humans; however, when human infection and subsequent human-to-human transmission occurs, worldwide outbreaks (pandemics) can result. The recent sporadic infections of humans in China with a previously unrecognized avian influenza A virus of the H7N9 subtype (A(H7N9)) have caused concern owing to the appreciable case fatality rate associated with these infections (more than 25%), potential instances of human-to-human transmission
1
, and the lack of pre-existing immunity among humans to viruses of this subtype. Here we characterize two early human A(H7N9) isolates, A/Anhui/1/2013 (H7N9) and A/Shanghai/1/2013 (H7N9); hereafter referred to as Anhui/1 and Shanghai/1, respectively. In mice, Anhui/1 and Shanghai/1 were more pathogenic than a control avian H7N9 virus (A/duck/Gunma/466/2011 (H7N9); Dk/GM466) and a representative pandemic 2009 H1N1 virus (A/California/4/2009 (H1N1pdm09); CA04). Anhui/1, Shanghai/1 and Dk/GM466 replicated well in the nasal turbinates of ferrets. In nonhuman primates, Anhui/1 and Dk/GM466 replicated efficiently in the upper and lower respiratory tracts, whereas the replicative ability of conventional human influenza viruses is typically restricted to the upper respiratory tract of infected primates. By contrast, Anhui/1 did not replicate well in miniature pigs after intranasal inoculation. Critically, Anhui/1 transmitted through respiratory droplets in one of three pairs of ferrets. Glycan arrays showed that Anhui/1, Shanghai/1 and A/Hangzhou/1/2013 (H7N9) (a third human A(H7N9) virus tested in this assay) bind to human virus-type receptors, a property that may be critical for virus transmissibility in ferrets. Anhui/1 was found to be less sensitive in mice to neuraminidase inhibitors than a pandemic H1N1 2009 virus, although both viruses were equally susceptible to an experimental antiviral polymerase inhibitor. The robust replicative ability in mice, ferrets and nonhuman primates and the limited transmissibility in ferrets of Anhui/1 suggest that A(H7N9) viruses have pandemic potential. |
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| AbstractList | Here, biological attributes of two early human isolates of the newly emerged H7N9 influenza viruses are characterized: the potential of these viruses to infect and/or transmit within various animal models is discussed, as is their relative sensitivity to neuraminidase inhibitors and experimental polymerase inhibitors compared to an H1N1 pandemic strain.
Transmission of emerging H7N9 virus
By 20 July 2013, there had been 134 laboratory-confirmed human cases of infection with avian influenza A H7N9 virus infection, including 43 deaths.
Yoshihiro Kawaoka and colleagues characterize the biology of two recent isolates of the virus. They provide a wealth of data from infections in mice, pigs, macaques and ferrets. H7N9 virus is shown to be less sensitive to neuraminidase inhibitors than pandemic H1N1 virus, but equally susceptible to an experimental polymerase inhibitor. Terrence Tumpey and colleagues determine the capacity of two clinical H7N9 isolates to cause disease and transmit between mammals. They show that the virus can replicate in human airway cells and in the respiratory tract of ferrets to a higher level than can seasonal H3N2 virus, and show higher lethality in mice than genetically related H7N9 and H9N2 viruses. In transmission studies, the H7N9 virus showed limited transmission in ferrets by respiratory droplets. Ron Fouchier and colleagues investigate the transmissibility of H7N9 virus between ferrets. They show that airborne transmission can occur, but inefficiently. They also show that on passage in ferrets, virus variants that have higher avian receptor binding, higher pH of fusion and lower thermostability are selected, and they suggest that these characteristics may result in reduced transmissibility.
Avian influenza A viruses rarely infect humans; however, when human infection and subsequent human-to-human transmission occurs, worldwide outbreaks (pandemics) can result. The recent sporadic infections of humans in China with a previously unrecognized avian influenza A virus of the H7N9 subtype (A(H7N9)) have caused concern owing to the appreciable case fatality rate associated with these infections (more than 25%), potential instances of human-to-human transmission
1
, and the lack of pre-existing immunity among humans to viruses of this subtype. Here we characterize two early human A(H7N9) isolates, A/Anhui/1/2013 (H7N9) and A/Shanghai/1/2013 (H7N9); hereafter referred to as Anhui/1 and Shanghai/1, respectively. In mice, Anhui/1 and Shanghai/1 were more pathogenic than a control avian H7N9 virus (A/duck/Gunma/466/2011 (H7N9); Dk/GM466) and a representative pandemic 2009 H1N1 virus (A/California/4/2009 (H1N1pdm09); CA04). Anhui/1, Shanghai/1 and Dk/GM466 replicated well in the nasal turbinates of ferrets. In nonhuman primates, Anhui/1 and Dk/GM466 replicated efficiently in the upper and lower respiratory tracts, whereas the replicative ability of conventional human influenza viruses is typically restricted to the upper respiratory tract of infected primates. By contrast, Anhui/1 did not replicate well in miniature pigs after intranasal inoculation. Critically, Anhui/1 transmitted through respiratory droplets in one of three pairs of ferrets. Glycan arrays showed that Anhui/1, Shanghai/1 and A/Hangzhou/1/2013 (H7N9) (a third human A(H7N9) virus tested in this assay) bind to human virus-type receptors, a property that may be critical for virus transmissibility in ferrets. Anhui/1 was found to be less sensitive in mice to neuraminidase inhibitors than a pandemic H1N1 2009 virus, although both viruses were equally susceptible to an experimental antiviral polymerase inhibitor. The robust replicative ability in mice, ferrets and nonhuman primates and the limited transmissibility in ferrets of Anhui/1 suggest that A(H7N9) viruses have pandemic potential. Here, biological attributes of two early human isolates of the newly emerged H7N9 influenza viruses are characterized: the potential of these viruses to infect and/or transmit within various animal models is discussed, as is their relative sensitivity to neuraminidase inhibitors and experimental polymerase inhibitors compared to an H1N1 pandemic strain. Avian influenza A viruses rarely infect humans, but if they do and transmit among them, worldwide outbreaks (pandemics) can result. The recent sporadic infections of humans in China with a previously unrecognized avian influenza A virus of the H7N9 subtype (A(H7N9)) have caused concern due to the appreciable case fatality rate associated with these infections (>25%), potential instances of human-to-human transmission 1 , and the lack of pre-existing immunity among humans to viruses of this subtype. Here, we therefore characterized two early human A(H7N9) isolates, A/Anhui/1/2013 and A/Shanghai/1/2013 (H7N9; hereafter referred to as Anhui/1 and Shanghai/1, respectively). In mice, Anhui/1 and Shanghai/1 were more pathogenic than a control avian H7N9 virus (A/duck/Gunma/466/2011; H7N9; Dk/GM466) and a representative pandemic 2009 H1N1 virus (A/California/04/2009; H1N1; CA04). Anhui/1, Shanghai/1, and Dk/GM466 replicated well in the nasal turbinates of ferrets. In nonhuman primates (NHPs), Anhui/1 and Dk/GM466 replicated efficiently in the upper and lower respiratory tracts, whereas the replicative ability of conventional human influenza viruses is typically restricted to the upper respiratory tract of infected primates. By contrast, Anhui/1 did not replicate well in miniature pigs upon intranasal inoculation. Most critically, Anhui/1 transmitted via respiratory droplets in one of three pairs of ferrets. Glycan arrays demonstrated that Anhui/1, Shanghai/1, and A/Hangzhou/1/2013 (a third human A(H7N9) virus tested in this assay) bind to human virus-type receptors, a property that may be critical for virus transmissibility in ferrets. Anhui/1 was less sensitive than a pandemic 2009 H1N1 virus to neuraminidase inhibitors, although both viruses were equally susceptible to an experimental antiviral polymerase inhibitor. The robust replicative ability in mice, ferrets, and NHPs and the limited transmissibility in ferrets of Anhui/1 suggest that A(H7N9) viruses have pandemic potential. Avian influenza A viruses rarely infect humans; however, when human infection and subsequent human-to-human transmission occurs, worldwide outbreaks (pandemics) can result. The recent sporadic infections of humans in China with a previously unrecognized avian influenza A virus of the H7N9 subtype (A(H7N9)) have caused concern owing to the appreciable case fatality rate associated with these infections (more than 25%), potential instances of human-to-human transmission, and the lack of pre-existing immunity among humans to viruses of this subtype. Here we characterize two early human A(H7N9) isolates, A/Anhui/1/2013 (H7N9) and A/Shanghai/1/2013 (H7N9); hereafter referred to as Anhui/1 and Shanghai/1, respectively. In mice, Anhui/1 and Shanghai/1 were more pathogenic than a control avian H7N9 virus (A/duck/Gunma/466/2011 (H7N9); Dk/GM466) and a representative pandemic 2009 H1N1 virus (A/California/4/2009 (H1N1pdm09); CA04). Anhui/1, Shanghai/1 and Dk/GM466 replicated well in the nasal turbinates of ferrets. In nonhuman primates, Anhui/1 and Dk/GM466 replicated efficiently in the upper and lower respiratory tracts, whereas the replicative ability of conventional human influenza viruses is typically restricted to the upper respiratory tract of infected primates. By contrast, Anhui/1 did not replicate well in miniature pigs after intranasal inoculation. Critically, Anhui/1 transmitted through respiratory droplets in one of three pairs of ferrets. Glycan arrays showed that Anhui/1, Shanghai/1 and A/Hangzhou/1/2013 (H7N9) (a third human A(H7N9) virus tested in this assay) bind to human virus-type receptors, a property that may be critical for virus transmissibility in ferrets. Anhui/1 was found to be less sensitive in mice to neuraminidase inhibitors than a pandemic H1N1 2009 virus, although both viruses were equally susceptible to an experimental antiviral polymerase inhibitor. The robust replicative ability in mice, ferrets and nonhuman primates and the limited transmissibility in ferrets of Anhui/1 suggest that A(H7N9) viruses have pandemic potential. Avian influenza A viruses rarely infect humans; however, when human infection and subsequent human-to-human transmission occurs, worldwide outbreaks (pandemics) can result. The recent sporadic infections of humans in China with a previously unrecognized avian influenza A virus of the H7N9 subtype (A(H7N9)) have caused concern owing to the appreciable case fatality rate associated with these infections (more than 25%), potential instances of human-to-human transmission, and the lack of pre-existing immunity among humans to viruses of this subtype. Here we characterize two early human A(H7N9) isolates, A/Anhui/1/2013 (H7N9) and A/Shanghai/1/2013 (H7N9); hereafter referred to as Anhui/1 and Shanghai/1, respectively. In mice, Anhui/1 and Shanghai/1 were more pathogenic than a control avian H7N9 virus (A/duck/Gunma/466/2011 (H7N9); Dk/GM466) and a representative pandemic 2009 H1N1 virus (A/California/4/2009 (H1N1pdm09); CA04). Anhui/1, Shanghai/1 and Dk/GM466 replicated well in the nasal turbinates of ferrets. In nonhuman primates, Anhui/1 and Dk/GM466 replicated efficiently in the upper and lower respiratory tracts, whereas the replicative ability of conventional human influenza viruses is typically restricted to the upper respiratory tract of infected primates. By contrast, Anhui/1 did not replicate well in miniature pigs after intranasal inoculation. Critically, Anhui/1 transmitted through respiratory droplets in one of three pairs of ferrets. Glycan arrays showed that Anhui/1, Shanghai/1 and A/Hangzhou/1/2013 (H7N9) (a third human A(H7N9) virus tested in this assay) bind to human virus-type receptors, a property that may be critical for virus transmissibility in ferrets. Anhui/1 was found to be less sensitive in mice to neuraminidase inhibitors than a pandemic H1N1 2009 virus, although both viruses were equally susceptible to an experimental antiviral polymerase inhibitor. The robust replicative ability in mice, ferrets and nonhuman primates and the limited transmissibility in ferrets of Anhui/1 suggest that A(H7N9) viruses have pandemic potential.Avian influenza A viruses rarely infect humans; however, when human infection and subsequent human-to-human transmission occurs, worldwide outbreaks (pandemics) can result. The recent sporadic infections of humans in China with a previously unrecognized avian influenza A virus of the H7N9 subtype (A(H7N9)) have caused concern owing to the appreciable case fatality rate associated with these infections (more than 25%), potential instances of human-to-human transmission, and the lack of pre-existing immunity among humans to viruses of this subtype. Here we characterize two early human A(H7N9) isolates, A/Anhui/1/2013 (H7N9) and A/Shanghai/1/2013 (H7N9); hereafter referred to as Anhui/1 and Shanghai/1, respectively. In mice, Anhui/1 and Shanghai/1 were more pathogenic than a control avian H7N9 virus (A/duck/Gunma/466/2011 (H7N9); Dk/GM466) and a representative pandemic 2009 H1N1 virus (A/California/4/2009 (H1N1pdm09); CA04). Anhui/1, Shanghai/1 and Dk/GM466 replicated well in the nasal turbinates of ferrets. In nonhuman primates, Anhui/1 and Dk/GM466 replicated efficiently in the upper and lower respiratory tracts, whereas the replicative ability of conventional human influenza viruses is typically restricted to the upper respiratory tract of infected primates. By contrast, Anhui/1 did not replicate well in miniature pigs after intranasal inoculation. Critically, Anhui/1 transmitted through respiratory droplets in one of three pairs of ferrets. Glycan arrays showed that Anhui/1, Shanghai/1 and A/Hangzhou/1/2013 (H7N9) (a third human A(H7N9) virus tested in this assay) bind to human virus-type receptors, a property that may be critical for virus transmissibility in ferrets. Anhui/1 was found to be less sensitive in mice to neuraminidase inhibitors than a pandemic H1N1 2009 virus, although both viruses were equally susceptible to an experimental antiviral polymerase inhibitor. The robust replicative ability in mice, ferrets and nonhuman primates and the limited transmissibility in ferrets of Anhui/1 suggest that A(H7N9) viruses have pandemic potential. |
| Audience | Academic |
| Author | Saito, Takehiko Uraki, Ryuta Uchida, Yuko Yamayoshi, Seiya de Vries, Robert P. Odagiri, Takato Tomita, Yuriko Imai, Masaki Goto, Kazue Tamura, Tomokazu Maher, Eileen A. Okamatsu, Masatoshi McBride, Ryan Sugita, Yukihiko Sakai-Tagawa, Yuko Eisfeld, Amie J. Kishida, Noriko Ito, Mutsumi Yamada, Shinya Fan, Shufang Ozawa, Makoto Murakami, Shin Hanson, Anthony Takashita, Emi Shirakura, Masayuki Kawakami, Eiryo Fujimoto, Naomi Watanabe, Tokiko Nakajima, Noriko Zhong, Gongxun Katsura, Hiroaki Tashiro, Masato Ishikawa, Izumi Sakoda, Yoshihiro Watanabe, Shinji Shichinohe, Shintaro Iwatsuki-Horimoto, Kiyoko Kiso, Maki Fukuyama, Satoshi Noda, Takeshi Imai, Hirotaka Kawaoka, Yoshihiro Hatta, Masato Neumann, Gabriele Zhao, Dongming Yamaji, Reina Paulson, James C. Kida, Hiroshi Hasegawa, Hideki Ping, Jihui |
| AuthorAffiliation | 13 Research Center for Zoonosis Control, Hokkaido University, Sapporo 001-0020, Japan 2 Division of Virology, Department of Microbiology and Immunology, Institute of Medical Science, University of Tokyo, Tokyo 108-8639, Japan 14 Laboratory of Bioresponses Regulation, Department of Biological Responses, Institute for Virus Research, Kyoto University, Kyoto 606-8507, Japan 10 Influenza and Prion Disease Research Center, National Institute of Animal Health, Kannondai 3-1-5, Tsukuba, Ibaraki, 305-0856 Japan 9 Laboratory of Veterinary Microbiology, Department of Veterinary Sciences, University of Miyazaki, Miyazaki, 889-2192, Japan 12 Transboundary Animal Distance Center, Joint Faculty of Veterinary Medicine, Kagoshima University, Kagoshima 890-0065, Japan 7 The Scripps Research Institute, 10550 North Torrey Pines Road, SP-3 La Jolla, CA 92037, USA 1 ERATO Infection-Induced Host Responses Project, Japan Science and Technology Agency, Saitama 332-0012, Japan 3 Department of Pathology, National Insti |
| AuthorAffiliation_xml | – name: 14 Laboratory of Bioresponses Regulation, Department of Biological Responses, Institute for Virus Research, Kyoto University, Kyoto 606-8507, Japan – name: 9 Laboratory of Veterinary Microbiology, Department of Veterinary Sciences, University of Miyazaki, Miyazaki, 889-2192, Japan – name: 11 Laboratory of Animal Hygiene, Joint Faculty of Veterinary Medicine, Kagoshima University, Kagoshima 890-0065, Japan – name: 1 ERATO Infection-Induced Host Responses Project, Japan Science and Technology Agency, Saitama 332-0012, Japan – name: 5 Department of Special Pathogens, International Research Center for Infectious Diseases, Institute of Medical Science, University of Tokyo, Minato-ku, Tokyo 108-8639, Japan – name: 6 Laboratory of Microbiology, Department of Disease Control, Graduate School of Veterinary Medicine, Hokkaido University, Sapporo 060-0818, Japan – name: 10 Influenza and Prion Disease Research Center, National Institute of Animal Health, Kannondai 3-1-5, Tsukuba, Ibaraki, 305-0856 Japan – name: 3 Department of Pathology, National Institute of Infectious Diseases, Shinjuku, Tokyo 162-8640, Japan – name: 7 The Scripps Research Institute, 10550 North Torrey Pines Road, SP-3 La Jolla, CA 92037, USA – name: 12 Transboundary Animal Distance Center, Joint Faculty of Veterinary Medicine, Kagoshima University, Kagoshima 890-0065, Japan – name: 13 Research Center for Zoonosis Control, Hokkaido University, Sapporo 001-0020, Japan – name: 4 Influenza Virus Research Center, National Institute of Infectious Diseases, Musashimurayama, Tokyo 208-0011, Japan – name: 8 Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin-Madison, 575 Science Drive, Madison, WI 53711, USA – name: 2 Division of Virology, Department of Microbiology and Immunology, Institute of Medical Science, University of Tokyo, Tokyo 108-8639, Japan |
| Author_xml | – sequence: 1 givenname: Tokiko surname: Watanabe fullname: Watanabe, Tokiko organization: ERATO Infection-Induced Host Responses Project, Japan Science and Technology Agency, Saitama 332-0012, Japan – sequence: 2 givenname: Maki surname: Kiso fullname: Kiso, Maki organization: Division of Virology, Department of Microbiology and Immunology, Institute of Medical Science, University of Tokyo, Tokyo 108-8639, Japan – sequence: 3 givenname: Satoshi surname: Fukuyama fullname: Fukuyama, Satoshi organization: ERATO Infection-Induced Host Responses Project, Japan Science and Technology Agency, Saitama 332-0012, Japan – sequence: 4 givenname: Noriko surname: Nakajima fullname: Nakajima, Noriko organization: Department of Pathology, National Institute of Infectious Diseases, Shinjuku, Tokyo 162-8640, Japan – sequence: 5 givenname: Masaki surname: Imai fullname: Imai, Masaki organization: Influenza Virus Research Center, National Institute of Infectious Diseases, Musashimurayama, Tokyo 208-0011, Japan – sequence: 6 givenname: Shinya surname: Yamada fullname: Yamada, Shinya organization: Division of Virology, Department of Microbiology and Immunology, Institute of Medical Science, University of Tokyo, Tokyo 108-8639, Japan – sequence: 7 givenname: Shin surname: Murakami fullname: Murakami, Shin organization: Department of Special Pathogens, International Research Center for Infectious Diseases, Institute of Medical Science, University of Tokyo, Minato-ku, Tokyo 108-8639, Japan – sequence: 8 givenname: Seiya surname: Yamayoshi fullname: Yamayoshi, Seiya organization: Division of Virology, Department of Microbiology and Immunology, Institute of Medical Science, University of Tokyo, Tokyo 108-8639, Japan – sequence: 9 givenname: Kiyoko surname: Iwatsuki-Horimoto fullname: Iwatsuki-Horimoto, Kiyoko organization: Division of Virology, Department of Microbiology and Immunology, Institute of Medical Science, University of Tokyo, Tokyo 108-8639, Japan – sequence: 10 givenname: Yoshihiro surname: Sakoda fullname: Sakoda, Yoshihiro organization: Department of Disease Control, Laboratory of Microbiology, Graduate School of Veterinary Medicine, Hokkaido University, Sapporo 060-0818, Japan – sequence: 11 givenname: Emi surname: Takashita fullname: Takashita, Emi organization: Influenza Virus Research Center, National Institute of Infectious Diseases, Musashimurayama, Tokyo 208-0011, Japan – sequence: 12 givenname: Ryan surname: McBride fullname: McBride, Ryan organization: The Scripps Research Institute, 10550 North Torrey Pines Road – sequence: 13 givenname: Takeshi surname: Noda fullname: Noda, Takeshi organization: Division of Virology, Department of Microbiology and Immunology, Institute of Medical Science, University of Tokyo, Tokyo 108-8639, Japan – sequence: 14 givenname: Masato surname: Hatta fullname: Hatta, Masato organization: Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin-Madison, 575 Science Drive, Madison, Wisconsin 53711, USA – sequence: 15 givenname: Hirotaka surname: Imai fullname: Imai, Hirotaka organization: Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin-Madison, 575 Science Drive, Madison, Wisconsin 53711, USA – sequence: 16 givenname: Dongming surname: Zhao fullname: Zhao, Dongming organization: ERATO Infection-Induced Host Responses Project, Japan Science and Technology Agency, Saitama 332-0012, Japan – sequence: 17 givenname: Noriko surname: Kishida fullname: Kishida, Noriko organization: Influenza Virus Research Center, National Institute of Infectious Diseases, Musashimurayama, Tokyo 208-0011, Japan – sequence: 18 givenname: Masayuki surname: Shirakura fullname: Shirakura, Masayuki organization: Influenza Virus Research Center, National Institute of Infectious Diseases, Musashimurayama, Tokyo 208-0011, Japan – sequence: 19 givenname: Robert P. surname: de Vries fullname: de Vries, Robert P. organization: The Scripps Research Institute, 10550 North Torrey Pines Road – sequence: 20 givenname: Shintaro surname: Shichinohe fullname: Shichinohe, Shintaro organization: Department of Disease Control, Laboratory of Microbiology, Graduate School of Veterinary Medicine, Hokkaido University, Sapporo 060-0818, Japan – sequence: 21 givenname: Masatoshi surname: Okamatsu fullname: Okamatsu, Masatoshi organization: Department of Disease Control, Laboratory of Microbiology, Graduate School of Veterinary Medicine, Hokkaido University, Sapporo 060-0818, Japan – sequence: 22 givenname: Tomokazu surname: Tamura fullname: Tamura, Tomokazu organization: Department of Disease Control, Laboratory of Microbiology, Graduate School of Veterinary Medicine, Hokkaido University, Sapporo 060-0818, Japan – sequence: 23 givenname: Yuriko surname: Tomita fullname: Tomita, Yuriko organization: ERATO Infection-Induced Host Responses Project, Japan Science and Technology Agency, Saitama 332-0012, Japan – sequence: 24 givenname: Naomi surname: Fujimoto fullname: Fujimoto, Naomi organization: ERATO Infection-Induced Host Responses Project, Japan Science and Technology Agency, Saitama 332-0012, Japan – sequence: 25 givenname: Kazue surname: Goto fullname: Goto, Kazue organization: ERATO Infection-Induced Host Responses Project, Japan Science and Technology Agency, Saitama 332-0012, Japan – sequence: 26 givenname: Hiroaki surname: Katsura fullname: Katsura, Hiroaki organization: Division of Virology, Department of Microbiology and Immunology, Institute of Medical Science, University of Tokyo, Tokyo 108-8639, Japan – sequence: 27 givenname: Eiryo surname: Kawakami fullname: Kawakami, Eiryo organization: ERATO Infection-Induced Host Responses Project, Japan Science and Technology Agency, Saitama 332-0012, Japan – sequence: 28 givenname: Izumi surname: Ishikawa fullname: Ishikawa, Izumi organization: ERATO Infection-Induced Host Responses Project, Japan Science and Technology Agency, Saitama 332-0012, Japan – sequence: 29 givenname: Shinji surname: Watanabe fullname: Watanabe, Shinji organization: ERATO Infection-Induced Host Responses Project, Japan Science and Technology Agency, Saitama 332-0012, Japan, Department of Veterinary Sciences, Laboratory of Veterinary Microbiology, University of Miyazaki, Miyazaki 889-2192, Japan – sequence: 30 givenname: Mutsumi surname: Ito fullname: Ito, Mutsumi organization: Division of Virology, Department of Microbiology and Immunology, Institute of Medical Science, University of Tokyo, Tokyo 108-8639, Japan – sequence: 31 givenname: Yuko surname: Sakai-Tagawa fullname: Sakai-Tagawa, Yuko organization: Division of Virology, Department of Microbiology and Immunology, Institute of Medical Science, University of Tokyo, Tokyo 108-8639, Japan – sequence: 32 givenname: Yukihiko surname: Sugita fullname: Sugita, Yukihiko organization: Division of Virology, Department of Microbiology and Immunology, Institute of Medical Science, University of Tokyo, Tokyo 108-8639, Japan – sequence: 33 givenname: Ryuta surname: Uraki fullname: Uraki, Ryuta organization: Division of Virology, Department of Microbiology and Immunology, Institute of Medical Science, University of Tokyo, Tokyo 108-8639, Japan – sequence: 34 givenname: Reina surname: Yamaji fullname: Yamaji, Reina organization: Division of Virology, Department of Microbiology and Immunology, Institute of Medical Science, University of Tokyo, Tokyo 108-8639, Japan – sequence: 35 givenname: Amie J. surname: Eisfeld fullname: Eisfeld, Amie J. organization: Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin-Madison, 575 Science Drive, Madison, Wisconsin 53711, USA – sequence: 36 givenname: Gongxun surname: Zhong fullname: Zhong, Gongxun organization: Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin-Madison, 575 Science Drive, Madison, Wisconsin 53711, USA – sequence: 37 givenname: Shufang surname: Fan fullname: Fan, Shufang organization: Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin-Madison, 575 Science Drive, Madison, Wisconsin 53711, USA – sequence: 38 givenname: Jihui surname: Ping fullname: Ping, Jihui organization: Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin-Madison, 575 Science Drive, Madison, Wisconsin 53711, USA – sequence: 39 givenname: Eileen A. surname: Maher fullname: Maher, Eileen A. organization: Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin-Madison, 575 Science Drive, Madison, Wisconsin 53711, USA – sequence: 40 givenname: Anthony surname: Hanson fullname: Hanson, Anthony organization: Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin-Madison, 575 Science Drive, Madison, Wisconsin 53711, USA – sequence: 41 givenname: Yuko surname: Uchida fullname: Uchida, Yuko organization: Influenza and Prion Disease Research Center, National Institute of Animal Health, Kannondai 3-1-5, Tsukuba, Ibaraki 305-0856, Japan – sequence: 42 givenname: Takehiko surname: Saito fullname: Saito, Takehiko organization: Influenza and Prion Disease Research Center, National Institute of Animal Health, Kannondai 3-1-5, Tsukuba, Ibaraki 305-0856, Japan – sequence: 43 givenname: Makoto surname: Ozawa fullname: Ozawa, Makoto organization: Laboratory of Animal Hygiene, Joint Faculty of Veterinary Medicine, Kagoshima University, Kagoshima 890-0065, Japan, Transboundary Animal Disease Center, Joint Faculty of Veterinary Medicine, Kagoshima University, Kagoshima 890-0065, Japan – sequence: 44 givenname: Gabriele surname: Neumann fullname: Neumann, Gabriele organization: Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin-Madison, 575 Science Drive, Madison, Wisconsin 53711, USA – sequence: 45 givenname: Hiroshi surname: Kida fullname: Kida, Hiroshi organization: Department of Disease Control, Laboratory of Microbiology, Graduate School of Veterinary Medicine, Hokkaido University, Sapporo 060-0818, Japan, Research Center for Zoonosis Control, Hokkaido University, Sapporo 001-0020, Japan – sequence: 46 givenname: Takato surname: Odagiri fullname: Odagiri, Takato organization: Influenza Virus Research Center, National Institute of Infectious Diseases, Musashimurayama, Tokyo 208-0011, Japan – sequence: 47 givenname: James C. surname: Paulson fullname: Paulson, James C. organization: The Scripps Research Institute, 10550 North Torrey Pines Road – sequence: 48 givenname: Hideki surname: Hasegawa fullname: Hasegawa, Hideki organization: Department of Pathology, National Institute of Infectious Diseases, Shinjuku, Tokyo 162-8640, Japan – sequence: 49 givenname: Masato surname: Tashiro fullname: Tashiro, Masato organization: Influenza Virus Research Center, National Institute of Infectious Diseases, Musashimurayama, Tokyo 208-0011, Japan – sequence: 50 givenname: Yoshihiro surname: Kawaoka fullname: Kawaoka, Yoshihiro email: kawaokay@svm.vetmed.wisc.edu organization: ERATO Infection-Induced Host Responses Project, Japan Science and Technology Agency, Saitama 332-0012, Japan, Division of Virology, Department of Microbiology and Immunology, Institute of Medical Science, University of Tokyo, Tokyo 108-8639, Japan, Department of Special Pathogens, International Research Center for Infectious Diseases, Institute of Medical Science, University of Tokyo, Minato-ku, Tokyo 108-8639, Japan, Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin-Madison, 575 Science Drive, Madison, Wisconsin 53711, USA, Department of Biological Responses, Laboratory of Bioresponses Regulation, Institute for Virus Research, Kyoto University, Kyoto 606-8507, Japan |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/23842494$$D View this record in MEDLINE/PubMed |
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USA199996934593501:CAS:528:DyaK1MXltVCjsrk%3D1999PNAS...96.9345N10.1073/pnas.96.16.9345 van den BrandJMSeverity of pneumonia due to new H1N1 influenza virus in ferrets is intermediate between that due to seasonal H1N1 virus and highly pathogenic avian influenza H5N1 virusJ. Infect. Dis.201020199399910.1086/651132 Centers for Disease Control & PreventionEmergence of avian influenza A(H7N9) virus causing severe human illness - China, February–April 2013MMWR Morb. Mortal. 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Microbiol.2003417427501:CAS:528:DC%2BD3sXhslGitLk%3D10.1128/JCM.41.2.742-750.2003 – reference: ChandrasekaranAGlycan topology determines human adaptation of avian H5N1 virus hemagglutininNature Biotechnol.2008261071131:CAS:528:DC%2BD1cXisFGmtA%3D%3D10.1038/nbt1375 – reference: LiuXPoor responses to oseltamivir treatment in a patient with influenza A (H7N9) virus infectionEmerg. Microbes & Infections20132e27 – reference: MainesTRTransmission and pathogenesis of swine-origin 2009 A(H1N1) influenza viruses in ferrets and miceScience20093254844871:CAS:528:DC%2BD1MXovVCgtLw%3D2009Sci...325..484M10.1126/science.1177238 – reference: McKimm-BreschkinJLMutations in a conserved residue in the influenza virus neuraminidase active site decreases sensitivity to Neu5Ac2en-derived inhibitorsJ. Virol.199872245624621:CAS:528:DyaK1cXhtFegtrk%3D9499107109546 – reference: JakielaBBrockman-SchneiderRAminevaSLeeWMGernJEBasal cells of differentiated bronchial epithelium are more susceptible to rhinovirus infectionAm. J. Respir. Cell Mol. Biol.2008385175231:CAS:528:DC%2BD1cXlvFWksrg%3D10.1165/rcmb.2007-0050OC – reference: ItohYIn vitro and in vivo characterization of new swine-origin H1N1 influenza virusesNature2009460102110251:CAS:528:DC%2BD1MXhtVWhsbvJ2009Natur.460.1021I10.1038/nature08260 – reference: HerfstSAirborne transmission of influenza A/H5N1 virus between ferretsScience2012336153415411:CAS:528:DC%2BC38Xoslaksbw%3D2012Sci...336.1534H10.1126/science.1213362 – reference: MakarovaNVOzakiHKidaHWebsterRGPerezDRReplication and transmission of influenza viruses in Japanese quailVirology20033108151:CAS:528:DC%2BD3sXkt1yjtrY%3D10.1016/S0042-6822(03)00094-1 – reference: World Health Organization Number of confirmed human cases of avian influenza A(H7N9) reported to WHO. Report 8 – data in WHO/HQ as of 30 May 2013, 15:45 GMT+1. http://www.who.int/influenza/human_animal_interface/influenza_h7n9/08_ReportWebH7N9Number.pdf (2013) – reference: YamadaSHaemagglutinin mutations responsible for the binding of H5N1 influenza A viruses to human-type receptorsNature20064443783821:CAS:528:DC%2BD28Xht1Sgtb7J2006Natur.444..378Y10.1038/nature05264 – reference: NiwaHYamamuraKMiyazakiJEfficient selection for high-expression transfectants with a novel eukaryotic vectorGene19911081931991:CAS:528:DyaK38Xlt1GksA%3D%3D10.1016/0378-1119(91)90434-D – reference: HattaMGaoPHalfmannPKawaokaYMolecular basis for high virulence of Hong Kong H5N1 influenza A virusesScience2001293184018421:CAS:528:DC%2BD3MXmvVSktrw%3D2001Sci...293.1840H10.1126/science.1062882 – reference: Zhu, H. et al. Infectivity, transmission, and pathology of human H7N9 influenza in ferrets and pigs. 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(2013) – reference: LiuJHighly pathogenic H5N1 influenza virus infection in migratory birdsScience200530912061:CAS:528:DC%2BD2MXovV2itrk%3D2005Sci...309.1210L10.1126/science.1115273 – reference: BelserJAContemporary North American influenza H7 viruses possess human receptor specificity: implications for virus transmissibilityProc. Natl Acad. Sci. USA2008105755875631:CAS:528:DC%2BD1cXmvFKksLc%3D2008PNAS..105.7558B10.1073/pnas.0801259105 – reference: XuRA recurring motif for antibody recognition of the receptor-binding site of influenza hemagglutininNature Struct. Mol. Biol.2013203633701:CAS:528:DC%2BC3sXit1aiu7w%3D2013sg2..book.....X10.1038/nsmb.2500 – reference: Centers for Disease Control & PreventionEmergence of avian influenza A(H7N9) virus causing severe human illness - China, February–April 2013MMWR Morb. Mortal. Wkly Rep.201362366371 – reference: MunsterVJPathogenesis and transmission of swine-origin 2009 A(H1N1) influenza virus in ferretsScience20093254814831:CAS:528:DC%2BD1MXovVCgtL8%3D2009Sci...325..481M10.1126/science.1177127 – reference: SrinivasanKRamanRJayaramanAViswanathanKSasisekharanRQuantitative characterization of glycan-receptor binding of H9N2 influenza A virus hemagglutininPLoS ONE20138e595501:CAS:528:DC%2BC3sXntVKrsLc%3D2013PLoSO...859550S10.1371/journal.pone.0059550 – reference: NodaTArchitecture of ribonucleoprotein complexes in influenza A virus particlesNature20064394904921:CAS:528:DC%2BD28XntFWlsQ%3D%3D2006Natur.439..490N10.1038/nature04378 – reference: ChutinimitkulSIn vitro assessment of attachment pattern and replication efficiency of H5N1 influenza A viruses with altered receptor specificityJ. 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Dis.201020199399910.1086/651132 – reference: ChenLMIn vitro evolution of H5N1 avian influenza virus toward human-type receptor specificityVirology201242210311310.1016/j.virol.2011.10.006 – reference: ImaiMExperimental adaptation of an influenza H5 HA confers respiratory droplet transmission to a reassortant H5 HA/H1N1 virus in ferretsNature20124864204281:CAS:528:DC%2BC38XovFyrsLY%3D2012Natur.486..420I10.1038/nature10831 – reference: MainesTRLack of transmission of H5N1 avian-human reassortant influenza viruses in a ferret modelProc. Natl Acad. Sci. USA200610312121121261:CAS:528:DC%2BD28XotlyitL4%3D2006PNAS..10312121M10.1073/pnas.0605134103 – reference: NeumannGGeneration of influenza A viruses entirely from cloned cDNAsProc. Natl Acad. Sci. 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| Snippet | Here, biological attributes of two early human isolates of the newly emerged H7N9 influenza viruses are characterized: the potential of these viruses to infect... Avian influenza A viruses rarely infect humans; however, when human infection and subsequent human-to-human transmission occurs, worldwide outbreaks... Avian influenza A viruses rarely infect humans, but if they do and transmit among them, worldwide outbreaks (pandemics) can result. The recent sporadic... |
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| SubjectTerms | 631/326/596/1578 Analysis Animals Antiviral Agents - pharmacology Avian influenza viruses Cells, Cultured Chickens - virology Comparative analysis DNA-Directed RNA Polymerases - antagonists & inhibitors Dogs Enzyme Inhibitors - pharmacology Female Ferrets - virology Genetic aspects Humanities and Social Sciences Humans Identification and classification Influenza A virus - chemistry Influenza A virus - drug effects Influenza A virus - isolation & purification Influenza A virus - pathogenicity Influenza A Virus, H1N1 Subtype - drug effects Influenza A Virus, H1N1 Subtype - enzymology Influenza viruses Influenza, Human - drug therapy Influenza, Human - virology letter Macaca fascicularis - virology Madin Darby Canine Kidney Cells Male Mice Mice, Inbred BALB C Models, Molecular Monkey Diseases - pathology Monkey Diseases - virology multidisciplinary Neuraminidase - antagonists & inhibitors Neuraminidase inhibitors Orthomyxoviridae Infections - pathology Orthomyxoviridae Infections - transmission Orthomyxoviridae Infections - virology Pathology Patient outcomes Physiological aspects Quail - virology Science Swine - virology Swine, Miniature - virology Virus Replication - drug effects Zoonoses |
| Title | Characterization of H7N9 influenza A viruses isolated from humans |
| URI | https://link.springer.com/article/10.1038/nature12392 https://www.ncbi.nlm.nih.gov/pubmed/23842494 https://www.proquest.com/docview/1437582016 https://pubmed.ncbi.nlm.nih.gov/PMC3891892 |
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