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M Imai, T Watanabe, M Kiso, N Nakajima, S Yamayoshi, K Iwatsuki-Horimoto, M Hatta, S Yamada, M Ito, Y Sakai-Tagawa, M Shirakura, E Takashita, S Fujisaki, R McBride, AJ Thompson, K Takahashi, T Maemura, H Mitake, S Chiba, G Zhong, S Fan, K Oishi, A Yasuhara, K Takada, T Nakao, S Fukuyama, M Yamashita, TJS Lopes, G Neumann, T Odagiri, S Watanabe, Y Shu, JC Paulson, H Hasegawa and Y Kawaoka
Low pathogenic H7N9 influenza viruses have recently evolved to become highly pathogenic, raising concerns of a pandemic, particularly if these viruses acquire efficient human-to-human transmissibility. We compared a low pathogenic H7N9 virus with a highly pathogenic isolate, and two of its variants that represent neuraminidase inhibitor-sensitive and -resistant subpopulations detected within the isolate. The highly pathogenic H7N9 viruses replicated efficiently in mice, ferrets, and/or nonhuman primates, and were more pathogenic in mice and ferrets than the low pathogenic H7N9 virus, with the exception of the neuraminidase inhibitor-resistant virus, which showed mild-to-moderate attenuation. All viruses transmitted among ferrets via respiratory droplets, and the neuraminidase-sensitive variant killed several of the infected and exposed animals. Neuraminidase inhibitors showed limited effectiveness against these viruses in vivo, but the viruses were susceptible to a polymerase inhibitor. These results suggest that the highly pathogenic H7N9 virus has pandemic potential and should be closely monitored.
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Reassortment, Influenza pandemic, Neuraminidase, DNA, Microbiology, Virus, Avian influenza, Influenza
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