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      Characterization of H7N9 influenza A viruses isolated from humans

      research-article
      1 , 2 , 1 , 3 , 4 , 2 , 5 , 2 , 2 , 6 , 4 , 7 , 2 , 8 , 8 , 1 , 4 , 4 , 7 , 6 , 6 , 6 , 1 , 1 , 1 , 2 , 1 , 1 , 1 , 9 , 2 , 2 , 2 , 2 , 2 , 8 , 8 , 8 , 8 , 8 , 8 , 10 , 10 , 11 , 12 , 8 , 6 , 13 , 4 , 7 , 3 , 4 , 1 , 2 , 5 , 8 , 14
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          Summary

          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.

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          Most cited references24

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          Human Infection with a Novel Avian-Origin Influenza A (H7N9) Virus

          New England Journal of Medicine, 368(20), 1888-1897
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            Molecular basis for high virulence of Hong Kong H5N1 influenza A viruses.

            M Hatta (2001)
            In 1997, an H5N1 influenza A virus was transmitted from birds to humans in Hong Kong, killing 6 of the 18 people infected. When mice were infected with the human isolates, two virulence groups became apparent. Using reverse genetics, we showed that a mutation at position 627 in the PB2 protein influenced the outcome of infection in mice. Moreover, high cleavability of the hemagglutinin glycoprotein was an essential requirement for lethal infection.
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              Highly pathogenic H5N1 influenza virus infection in migratory birds.

              H5N1 avian influenza virus (AIV) has emerged as a pathogenic entity for a variety of species, including humans, in recent years. Here we report an outbreak among migratory birds on Lake Qinghaihu, China, in May and June 2005, in which more than a thousand birds were affected. Pancreatic necrosis and abnormal neurological symptoms were the major clinical features. Sequencing of the complete genomes of four H5N1 AIV strains revealed them to be reassortants related to a peregrine falcon isolate from Hong Kong and to have known highly pathogenic characteristics. Experimental animal infections reproduced typical highly pathogenic AIV infection symptoms and pathology.
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                Author and article information

                Journal
                0410462
                6011
                Nature
                Nature
                Nature
                0028-0836
                1476-4687
                27 September 2013
                10 July 2013
                26 September 2013
                26 March 2014
                : 501
                : 7468
                : 551-555
                Affiliations
                [1 ]ERATO Infection-Induced Host Responses Project, Japan Science and Technology Agency, Saitama 332-0012, Japan
                [2 ]Division of Virology, Department of Microbiology and Immunology, Institute of Medical Science, University of Tokyo, Tokyo 108-8639, Japan
                [3 ]Department of Pathology, National Institute of Infectious Diseases, Shinjuku, Tokyo 162-8640, Japan
                [4 ]Influenza Virus Research Center, National Institute of Infectious Diseases, Musashimurayama, Tokyo 208-0011, Japan
                [5 ]Department of Special Pathogens, International Research Center for Infectious Diseases, Institute of Medical Science, University of Tokyo, Minato-ku, Tokyo 108-8639, Japan
                [6 ]Laboratory of Microbiology, Department of Disease Control, Graduate School of Veterinary Medicine, Hokkaido University, Sapporo 060-0818, Japan
                [7 ]The Scripps Research Institute, 10550 North Torrey Pines Road, SP-3 La Jolla, CA 92037, USA
                [8 ]Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin-Madison, 575 Science Drive, Madison, WI 53711, USA
                [9 ]Laboratory of Veterinary Microbiology, Department of Veterinary Sciences, University of Miyazaki, Miyazaki, 889-2192, Japan
                [10 ]Influenza and Prion Disease Research Center, National Institute of Animal Health, Kannondai 3-1-5, Tsukuba, Ibaraki, 305-0856 Japan
                [11 ]Laboratory of Animal Hygiene, Joint Faculty of Veterinary Medicine, Kagoshima University, Kagoshima 890-0065, Japan
                [12 ]Transboundary Animal Distance Center, Joint Faculty of Veterinary Medicine, Kagoshima University, Kagoshima 890-0065, Japan
                [13 ]Research Center for Zoonosis Control, Hokkaido University, Sapporo 001-0020, Japan
                [14 ]Laboratory of Bioresponses Regulation, Department of Biological Responses, Institute for Virus Research, Kyoto University, Kyoto 606-8507, Japan
                Author notes
                Correspondence and requests for materials should be addressed to Y.K. ( kawaokay@ 123456svm.vetmed.wisc.edu )
                [*]

                These authors contributed equally to this work

                Article
                NIHMS496958
                10.1038/nature12392
                3891892
                23842494
                5d501581-05d9-4d3a-974a-18e27d85b86d

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