Biological features of novel avian influenza A (H7N9) virus
An initial characterization of the receptor-binding properties of the novel avian influenza A (H7N9) shows that the virus has acquired the ability to bind human receptors while retaining the ability to bind avian receptors; the virus infects epithelial cells in the human lower respiratory tract and...
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| Published in | Nature (London) Vol. 499; no. 7459; pp. 500 - 503 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
London
Nature Publishing Group UK
25.07.2013
Nature Publishing Group |
| Subjects | |
| Online Access | Get full text |
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| Abstract | An initial characterization of the receptor-binding properties of the novel avian influenza A (H7N9) shows that the virus has acquired the ability to bind human receptors while retaining the ability to bind avian receptors; the virus infects epithelial cells in the human lower respiratory tract and type II pneumocytes in the alveoli, and hypercytokinaemia was seen in infected patients.
H7N9 avian flu virus isolates examined
The H7N9 avian flu virus emerged in the human population on mainland China in February 2013, and by the first week of July WHO had recorded 133 cases including 43 deaths. Most cases so far have been linked to live bird markets. In this issue of
Nature
two groups report on the receptor-binding properties of H7N9. Both find that the virus has acquired the ability to bind the human α-2,3-linked sialic acid receptor yet has a retained preference for binding to the avian 2,3-linked receptor, a factor that may restrict its further evolution towards efficient transmission between humans. Steven Gamblin and colleagues also solve the crystal structure of the H7 haemagglutinin in complex with the receptor analogues, revealing details of how the human-receptor-binding properties may have arisen. Yuelong Shu and colleagues examine the pattern of virus infection in lung tissue. In human tracheal and lung explants, the virus infects epithelial cells in the lower respiratory tract and type II pneumocytes in the alveoli, and is better able to replicate in the lower respiratory tract compared with the trachea, a possible factor in the inefficient human-to-human transmission seen to date. They also report hypercytokinaemia in some patients — a cytokine storm that can contribute to disease severity — comparable to that seen in some H5N1 infections.
Human infection associated with a novel reassortant avian influenza H7N9 virus has recently been identified in China
1
. A total of 132 confirmed cases and 39 deaths have been reported
2
. Most patients presented with severe pneumonia and acute respiratory distress syndrome
3
,
4
. Although the first epidemic has subsided, the presence of a natural reservoir and the disease severity highlight the need to evaluate its risk on human public health and to understand the possible pathogenesis mechanism. Here we show that the emerging H7N9 avian influenza virus poses a potentially high risk to humans. We discover that the H7N9 virus can bind to both avian-type (α2,3-linked sialic acid) and human-type (α2,6-linked sialic acid) receptors. It can invade epithelial cells in the human lower respiratory tract and type II pneumonocytes in alveoli, and replicated efficiently in
ex vivo
lung and trachea explant culture and several mammalian cell lines. In acute serum samples of H7N9-infected patients, increased levels of the chemokines and cytokines IP-10, MIG, MIP-1β, MCP-1, IL-6, IL-8 and IFN-α were detected. We note that the human population is naive to the H7N9 virus, and current seasonal vaccination could not provide protection. |
|---|---|
| AbstractList | Human infection associated with a novel reassortant avian influenza H7N9 virus has recently been identified in China. A total of 132 confirmed cases and 39 deaths have been reported. Most patients presented with severe pneumonia and acute respiratory distress syndrome. Although the first epidemic has subsided, the presence of a natural reservoir and the disease severity highlight the need to evaluate its risk on human public health and to understand the possible pathogenesis mechanism. Here we show that the emerging H7N9 avian influenza virus poses a potentially high risk to humans. We discover that the H7N9 virus can bind to both avian-type (α2,3-linked sialic acid) and human-type (α2,6-linked sialic acid) receptors. It can invade epithelial cells in the human lower respiratory tract and type II pneumonocytes in alveoli, and replicated efficiently in ex vivo lung and trachea explant culture and several mammalian cell lines. In acute serum samples of H7N9-infected patients, increased levels of the chemokines and cytokines IP-10, MIG, MIP-1β, MCP-1, IL-6, IL-8 and IFN-α were detected. We note that the human population is naive to the H7N9 virus, and current seasonal vaccination could not provide protection. An initial characterization of the receptor-binding properties of the novel avian influenza A (H7N9) shows that the virus has acquired the ability to bind human receptors while retaining the ability to bind avian receptors; the virus infects epithelial cells in the human lower respiratory tract and type II pneumocytes in the alveoli, and hypercytokinaemia was seen in infected patients. H7N9 avian flu virus isolates examined The H7N9 avian flu virus emerged in the human population on mainland China in February 2013, and by the first week of July WHO had recorded 133 cases including 43 deaths. Most cases so far have been linked to live bird markets. In this issue of Nature two groups report on the receptor-binding properties of H7N9. Both find that the virus has acquired the ability to bind the human α-2,3-linked sialic acid receptor yet has a retained preference for binding to the avian 2,3-linked receptor, a factor that may restrict its further evolution towards efficient transmission between humans. Steven Gamblin and colleagues also solve the crystal structure of the H7 haemagglutinin in complex with the receptor analogues, revealing details of how the human-receptor-binding properties may have arisen. Yuelong Shu and colleagues examine the pattern of virus infection in lung tissue. In human tracheal and lung explants, the virus infects epithelial cells in the lower respiratory tract and type II pneumocytes in the alveoli, and is better able to replicate in the lower respiratory tract compared with the trachea, a possible factor in the inefficient human-to-human transmission seen to date. They also report hypercytokinaemia in some patients — a cytokine storm that can contribute to disease severity — comparable to that seen in some H5N1 infections. Human infection associated with a novel reassortant avian influenza H7N9 virus has recently been identified in China 1 . A total of 132 confirmed cases and 39 deaths have been reported 2 . Most patients presented with severe pneumonia and acute respiratory distress syndrome 3 , 4 . Although the first epidemic has subsided, the presence of a natural reservoir and the disease severity highlight the need to evaluate its risk on human public health and to understand the possible pathogenesis mechanism. Here we show that the emerging H7N9 avian influenza virus poses a potentially high risk to humans. We discover that the H7N9 virus can bind to both avian-type (α2,3-linked sialic acid) and human-type (α2,6-linked sialic acid) receptors. It can invade epithelial cells in the human lower respiratory tract and type II pneumonocytes in alveoli, and replicated efficiently in ex vivo lung and trachea explant culture and several mammalian cell lines. In acute serum samples of H7N9-infected patients, increased levels of the chemokines and cytokines IP-10, MIG, MIP-1β, MCP-1, IL-6, IL-8 and IFN-α were detected. We note that the human population is naive to the H7N9 virus, and current seasonal vaccination could not provide protection. Human infection associated with a novel reassortant avian influenza H7N9 virus has recently been identified in China. A total of 132 confirmed cases and 39 deaths have been reported. Most patients presented with severe pneumonia and acute respiratory distress syndrome. Although the first epidemic has subsided, the presence of a natural reservoir and the disease severity highlight the need to evaluate its risk on human public health and to understand the possible pathogenesis mechanism. Here we show that the emerging H7N9 avian influenza virus poses a potentially high risk to humans. We discover that the H7N9 virus can bind to both avian-type (α2,3-linked sialic acid) and human-type (α2,6-linked sialic acid) receptors. It can invade epithelial cells in the human lower respiratory tract and type II pneumonocytes in alveoli, and replicated efficiently in ex vivo lung and trachea explant culture and several mammalian cell lines. In acute serum samples of H7N9-infected patients, increased levels of the chemokines and cytokines IP-10, MIG, MIP-1β, MCP-1, IL-6, IL-8 and IFN-α were detected. We note that the human population is naive to the H7N9 virus, and current seasonal vaccination could not provide protection.Human infection associated with a novel reassortant avian influenza H7N9 virus has recently been identified in China. A total of 132 confirmed cases and 39 deaths have been reported. Most patients presented with severe pneumonia and acute respiratory distress syndrome. Although the first epidemic has subsided, the presence of a natural reservoir and the disease severity highlight the need to evaluate its risk on human public health and to understand the possible pathogenesis mechanism. Here we show that the emerging H7N9 avian influenza virus poses a potentially high risk to humans. We discover that the H7N9 virus can bind to both avian-type (α2,3-linked sialic acid) and human-type (α2,6-linked sialic acid) receptors. It can invade epithelial cells in the human lower respiratory tract and type II pneumonocytes in alveoli, and replicated efficiently in ex vivo lung and trachea explant culture and several mammalian cell lines. In acute serum samples of H7N9-infected patients, increased levels of the chemokines and cytokines IP-10, MIG, MIP-1β, MCP-1, IL-6, IL-8 and IFN-α were detected. We note that the human population is naive to the H7N9 virus, and current seasonal vaccination could not provide protection. An initial characterization of the receptor-binding properties of the novel avian influenza A (H7N9) shows that the virus has acquired the ability to bind human receptors while retaining the ability to bind avian receptors; the virus infects epithelial cells in the human lower respiratory tract and type II pneumocytes in the alveoli, and hypercytokinaemia was seen in infected patients. Human infection associated with a novel reassortant avian influenza H7N9 virus has recently been identified in China^sup 1^. A total of 132 confirmed cases and 39 deaths have been reported^sup 2^. Most patients presented with severe pneumonia and acute respiratory distress syndrome^sup 3,4^. Although the first epidemic has subsided, the presence of a natural reservoir and the disease severity highlight the need to evaluate its risk on human public health and to understand the possible pathogenesis mechanism. Here we show that the emerging H7N9 avian influenza virus poses a potentially high risk to humans. We discover that the H7N9 virus can bind to both avian - type (α2,3-linked sialic acid) and human-type (α2,6-linked sialic acid) receptors. It can invade epithelial cells in the human lower respiratory tract and type II pneumonocytes in alveoli, and replicated efficiently in ex vivo lung and trachea explant culture and several mammalian cell lines. In acute serum samples of H7N9-infected patients, increased levels of the chemokines and cytokines IP-10, MIG, MlP-1β, MCP-1, IL-6, IL-8 and IFN-α were detected. We note that the human population is naive to the H7N9 virus, and current seasonal vaccination could not provide protection. [PUBLICATION ABSTRACT] |
| Audience | Academic |
| Author | Liu, Liqi Yang, Weizhong Bai, Tian Qi, Xian Wang, Shiwen Shi, Yonglin Li, Xiaodan Chen, Yongkun Dong, Libo Huang, Weijuan Zhu, Wenfei Zhang, Xiaodong Gao, George F. Wang, Dayan Song, Jingdong Zhang, Ye Bo, Hong Guo, Junfeng Wen, Leying Han, Jun Xu, Cuilin Zhou, Jianfang Zhang, Yanjun Qin, Kun Lu, Jian Wang, Yu Gao, Rongbao Li, Xiyan Feng, Zijian Lan, Yu Li, Dexin Wei, Hejiang Dong, Jie Yang, Lei Wu, Guizhen Zou, Shumei Pei, Yuquan Zhao, Xiang Zhao, Baihui Xin, Li Yang, Yue Shu, Yuelong |
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and Prevention, China CDC, Key Laboratory for Medical Virology, National Health and Family Planning Commission – sequence: 6 givenname: Xian surname: Qi fullname: Qi, Xian organization: Jiangsu Provincial Disease Control and Prevention – sequence: 7 givenname: Yanjun surname: Zhang fullname: Zhang, Yanjun organization: Zhejiang Provincial Disease Control and Prevention – sequence: 8 givenname: Yonglin surname: Shi fullname: Shi, Yonglin organization: Anhui Provincial Disease Control and Prevention – sequence: 9 givenname: Lei surname: Yang fullname: Yang, Lei organization: National Institute for Viral Disease Control and Prevention, China CDC, Key Laboratory for Medical Virology, National Health and Family Planning Commission – sequence: 10 givenname: Wenfei surname: Zhu fullname: Zhu, Wenfei organization: National Institute for Viral Disease Control and Prevention, China CDC, Key Laboratory for Medical Virology, National Health and Family Planning Commission – sequence: 11 givenname: 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givenname: Li surname: Xin fullname: Xin, Li organization: National Institute for Viral Disease Control and Prevention, China CDC, Key Laboratory for Medical Virology, National Health and Family Planning Commission – sequence: 29 givenname: Yongkun surname: Chen fullname: Chen, Yongkun organization: National Institute for Viral Disease Control and Prevention, China CDC, Key Laboratory for Medical Virology, National Health and Family Planning Commission – sequence: 30 givenname: Cuilin surname: Xu fullname: Xu, Cuilin organization: National Institute for Viral Disease Control and Prevention, China CDC, Key Laboratory for Medical Virology, National Health and Family Planning Commission – sequence: 31 givenname: Yuquan surname: Pei fullname: Pei, Yuquan organization: Key laboratory of Carcinogenesis and Translational Research, Peking University Cancer Hospital – sequence: 32 givenname: Yue surname: Yang fullname: Yang, Yue organization: Key laboratory of Carcinogenesis and Translational Research, Peking University Cancer Hospital – sequence: 33 givenname: Xiaodong surname: Zhang fullname: Zhang, Xiaodong organization: Key laboratory of Carcinogenesis and Translational Research, Peking University Cancer Hospital – sequence: 34 givenname: Shiwen surname: Wang fullname: Wang, Shiwen organization: National Institute for Viral Disease Control and Prevention, China CDC, Key Laboratory for Medical Virology, National Health and Family Planning Commission – sequence: 35 givenname: Zijian surname: Feng fullname: Feng, Zijian organization: Chinese Center for Disease Control and Prevention – sequence: 36 givenname: Jun surname: Han fullname: Han, Jun organization: Chinese Center for Disease Control and Prevention – sequence: 37 givenname: Weizhong surname: Yang fullname: Yang, Weizhong organization: Chinese Center for Disease Control and Prevention – sequence: 38 givenname: George F. surname: Gao fullname: Gao, George F. organization: Chinese Center for Disease Control and Prevention – sequence: 39 givenname: Guizhen surname: Wu fullname: Wu, Guizhen organization: National Institute for Viral Disease Control and Prevention, China CDC, Key Laboratory for Medical Virology, National Health and Family Planning Commission – sequence: 40 givenname: Dexin surname: Li fullname: Li, Dexin organization: National Institute for Viral Disease Control and Prevention, China CDC, Key Laboratory for Medical Virology, National Health and Family Planning Commission – sequence: 41 givenname: Yu surname: Wang fullname: Wang, Yu organization: Chinese Center for Disease Control and Prevention – sequence: 42 givenname: Yuelong surname: Shu fullname: Shu, Yuelong email: yshu@cnic.org.cn organization: National Institute for Viral Disease Control and Prevention, China CDC, Key Laboratory for Medical Virology, National Health and Family Planning Commission |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/23823727$$D View this record in MEDLINE/PubMed |
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| Snippet | An initial characterization of the receptor-binding properties of the novel avian influenza A (H7N9) shows that the virus has acquired the ability to bind... Human infection associated with a novel reassortant avian influenza H7N9 virus has recently been identified in China. A total of 132 confirmed cases and 39... Human infection associated with a novel reassortant avian influenza H7N9 virus has recently been identified in China^sup 1^. A total of 132 confirmed cases and... |
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| SubjectTerms | 631/326/596/1578 Age Analysis Animals Antibodies, Viral - immunology Avian influenza Avian influenza viruses Biological complexity Birds - virology Bronchi - cytology Bronchi - metabolism Bronchi - virology Cell Line Chemokines Chemokines - blood China Cross Reactions - immunology Cytokines Distribution Epithelial Cells - virology Glycoproteins Health aspects Host Specificity Host-parasite relationships Human populations Humanities and Social Sciences Humans Identification and classification In Vitro Techniques Infections Influenza A virus - immunology Influenza A virus - pathogenicity Influenza A virus - physiology Influenza A Virus, H5N1 Subtype - immunology Influenza A Virus, H5N1 Subtype - physiology Influenza in Birds - transmission Influenza in Birds - virology Influenza Vaccines - immunology Influenza, Human - blood Influenza, Human - immunology Influenza, Human - virology letter Lung - virology multidisciplinary N-Acetylneuraminic Acid - analogs & derivatives N-Acetylneuraminic Acid - chemistry N-Acetylneuraminic Acid - metabolism Organ Specificity Pandemics Patient outcomes Physiological aspects Preferences Properties Protein binding Public health Pulmonary Alveoli - cytology Pulmonary Alveoli - metabolism Pulmonary Alveoli - virology Receptors, Virus - chemistry Receptors, Virus - metabolism Respiratory tract Science Trachea - virology Viral infections Virus Replication Viruses Zoonoses Zoonoses - transmission Zoonoses - virology |
| Title | Biological features of novel avian influenza A (H7N9) virus |
| URI | https://link.springer.com/article/10.1038/nature12379 https://www.ncbi.nlm.nih.gov/pubmed/23823727 https://www.proquest.com/docview/1426267678 https://www.proquest.com/docview/1413164355 |
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