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| 1 | H7N9 virulent mutants detected in chickens in China pose an increased threat to humans显示文摘 | Jianzhong Shi Guohua Deng Huihui Kong Chunyang Gu Shujie Ma Xin Yin Xianying Zeng Pengfei Cui Yan Chen Huanliang Yang Xiaopeng Wan Xiurong Wang Liling Liu Pucheng Chen Yongping Jiang Jinxiong Liu Yuntao Guan Yasuo Suzuki Mei Li Zhiyuan Qu Lizheng Guan Jinkai Zang Wenli Gu Shuyu Han Yangming Song Yuzhen Hu Zeng Wang Linlin Gu Wenyu Yang Libin Liang Hongmei Bao Guobin Tian Yanbing Li Chuanling Qiao Li Jiang Chengjun Li Zhigao Bu Hualan Chen | 2017 | Cell Research2017，27，12： | 70 |
| 2 | Vaccination of poultry successfully eliminated human infection with H7N9 virus in China显示文摘The H7 N9 viruses that emerged in China in 2013 were nonpathogenic in chickens but mutated to a highly pathogenic form in early 2017 and caused severe disease outbreaks in chickens. The H7 N9 influenza viruses have caused five waves of human infection, with almost half of the total number of human cases(766 of 1,567) being reported in the fifth wave, raising concerns that even more human infections could occur in the sixth wave. In September 2017, an H5/H7 bivalent inactivated vaccine for chickens was introduced, and the H7 N9 virus isolation rate in poultry dropped by 93.3% after vaccination. More importantly,only three H7 N9 human cases were reported between October 1, 2017 and September 30, 2018, indicating that vaccination of poultry successfully eliminated human infection with H7 N9 virus. These facts emphasize that active control of animal disease is extremely important for zoonosis control and human health protection. | Xianying Zeng Guobin Tian Jianzhong Shi Guohua Deng Chengjun Li Hualan Chen | 2018 | Science China(Life Sciences)2018，61，12： | 37 |
| 3 | Genetic and biological characteristics of the globally circulating H5N8 avian influenza viruses and the protective efficacy offered by the poultry vaccine currently used in China显示文摘The H5N8 avian influenza viruses have been widely circulating in wild birds and are responsible for the loss of over 33 million domestic poultry in Europe, Russia, Middle East, and Asia since January 2020. To monitor the invasion and spread of the H5N8 virus in China, we performed active surveillance by analyzing 317 wild bird samples and swab samples collected from 41,172 poultry all over the country. We isolated 22 H5N8 viruses from wild birds and 14 H5N8 viruses from waterfowls. Genetic analysis indicated that the 36 viruses formed two different genotypes: one genotype viruses were widely detected from different wild birds and domestic waterfowls;the other genotype was isolated from a whopper swan. We further revealed the origin and spatiotemporal spread of these two distinct H5N8 virus genotypes in 2020 and 2021. Animal studies indicated that the H5N8 isolates are highly pathogenic to chickens, mildly pathogenic in ducks, but have distinct pathotypes in mice. Moreover, we found that vaccinated poultry in China could be completely protected against H5N8 virus challenge. Given that the H5N8 viruses are likely to continue to spread in wild birds, vaccination of poultry is highly recommended in high-risk countries to prevent H5N8 avian influenza. | Pengfei Cui Xianying Zeng Xuyong Li Yanbing Li Jianzhong Shi Conghui Zhao Zhiyuan Qu Yanwen Wang Jing Guo Wenli Gu Qi Ma Yuancheng Zhang Weipeng Lin Minghui Li Jingman Tian Dongxue Wang Xin Xing Yanjing Liu Shuxin Pan Yaping Zhang Hongmei Bao Liling Liu Guobin Tian Chengjun Li Guohua Deng Hualan Chen | 2022 | Science China(Life Sciences)2022，65，4： | 12 |
| 4 | Influenza A virus use of BinCARD1 to facilitate the binding of viral NP to importinα7 is counteracted by TBK1-p62 axis-mediated autophagy显示文摘As a major component of the viral ribonucleoprotein(vRNP)complex in influenza A virus(IAV),nucleoprotein(NP)interacts with isoforms of importinαfamily members,leading to the import of itself and vRNP complex into the nucleus,a process pivotal in the replication cycle of IAV.In this study,we found that BinCARD1,an isoform of Bcl10-interacting protein with CARD(BinCARD),was leveraged by IAV for efficient viral replication.BinCARD1 promoted the nuclear import of the vRNP complex and newly synthesized NP and thus enhanced vRNP complex activity.Moreover,we found that BinCARD1 interacted with NP to promote NP binding to importinα7,an adaptor in the host nuclear import pathway.However,we also found that BinCARD1 promoted RIG-I-mediated innate immune signaling by mediating Lys63-linked polyubiquitination of TRAF3,and that TBK1 appeared to degrade BinCARD1.We showed that BinCARD1 was polyubiquitinated at residue K103 through a Lys63 linkage,which was recognized by the TBK1-p62 axis for autophagic degradation.Overall,our data demonstrate that IAV leverages BinCARD1 as an important host factor that promotes viral replication,and two mechanisms in the host defense system are triggered—innate immune signaling and autophagic degradation—to mitigate the promoting effect of BinCARD1 on the life cycle of IAV. | Xuyuan Wang Li Jiang Guangwen Wang Wenjun Shi Yuzhen Hu Bo Wang Xianying Zeng Guobin Tian Guohua Deng Jianzhong Shi Liling Liu Chengjun Li Hualan Chen | 2022 | Cellular & Molecular Immunology2022，19，10： | 3 |
| 5 | H7N9 virus infection triggers lethal cytokine storm by activating gasdermin E-mediated pyroptosis of lung alveolar epithelial cells显示文摘The H7N9 influenza virus emerged in China in 2013,causing more than 1560 human infections,39% of which were fatal.A ‘cytokine storm’ in the lungs of H7N9 patients has been linked to a poor prognosis and death;however,the underlying mechanism that triggers the cytokine storm is unknown.Here,we found that efficient replication of the H7N9 virus in mouse lungs activates gasdermin E(GSDME)-mediated pyroptosis in alveolar epithelial cells,and that the released cytosolic contents then trigger a cytokine storm.Knockout of Gsdme switched the manner of death of A549 and human primary alveolar epithelial cells from pyroptosis to apoptosis upon H7N9 virus infection,and Gsdme knockout mice survived H7N9 virus lethal infection.Our findings reveal that GSDME activation is a key and unique mechanism for the pulmonary cytokine storm and lethal outcome of H7N9 virus infection and thus opens a new door for the development of antivirals against the H7N9 virus. | Xiaopeng Wan Jiqing Li Yupeng Wang Xiaofei Yu Xijun He Jianzhong Shi Guohua Deng Xianying Zeng Guobin Tian Yanbing Li Yongping Jiang Yuntao Guan Chengjun Li Feng Shao Hualan Chen | 2022 | National Science Review2022，9，1： | 3 |
| 6 | Glycosylation and an amino acid insertion in the head of hemagglutinin independently affect the antigenic properties of H5N1 avian influenza viruses显示文摘Antigenic drift forces us to frequently update influenza vaccines; however, the genetic basis for antigenic variation remains largely unknown. In this study, we used clade 7.2 H5 viruses as models to explore the molecular determinants of influenza virus antigenic variation. We generated eight monoclonal antibodies(MAbs) targeted to the hemagglutinin(HA) protein of the index virus A/chicken/Shanxi/2/2006 and found that two representative antigenically drifted clade 7.2 viruses did not react with six of the eight MAbs. The E131 N mutation and insertion of leucine at position 134 in the HA protein of the antigenically drifted strains eliminated the reactivity of the virus with the MAbs. We also found that the amino acid N131 in the H5 HA protein is glycosylated. Our results provide experimental evidence that glycosylation and an amino acid insertion or deletion in HA influence antigenic variation. | Chunyang Gu Xianying Zeng Yangming Song Yanbing Li Liling Liu Yoshihiro Kawaoka Dongming Zhao Hualan Chen | 2019 | Science China(Life Sciences)2019，62，1： | 1 |
| 7 | Resistance Evaluation of Eggplant Resources to Verticillium Wilt in Sichuan Province 显示文摘 | Zeng Hualan Ye Pengsheng He Lian | 2009 | Agriculu- tral Science & Technology2009，10，12： | 1 |
| 8 | M6PR interacts with the HA2 subunit of influenza A virus to facilitate the fusion of viral and endosomal membranes显示文摘Influenza A virus(IAV) commandeers numerous host cellular factors for successful replication. However, very few host factors have been revealed to be involved in the fusion of viral envelope and late endosomal membranes. In this study, we identified cation-dependent mannose-6-phosphate receptor(M6PR) as a crucial host factor for the replication of IAV. We found that siRNA knockdown of M6PR expression significantly reduced the growth titers of different subtypes of IAV, and that the inhibitory effect of M6PR siRNA treatment on IAV growth was overcome by the complement of exogenously expressed M6PR. When A549 cells were treated with siRNA targeting M6PR,the nuclear accumulation of viral nucleoprotein(NP) was dramatically inhibited at early timepoints post-infection, indicating that M6PR engages in the early stage of the IAV replication cycle. By investigating the role of M6PR in the individual entry and post-entry steps of IAV replication, we found that the downregulation of M6PR expression had no effect on attachment, internalization, early endosome trafficking,or late endosome acidification. However, we found that M6PR expression was critical for the fusion of viral envelope and late endosomal membranes. Of note, M6PR interacted with the hemagglutinin(HA) protein of IAV, and further studies showed that the lumenal domain of M6PR and the ectodomain of HA2 mediated the interaction and directly promoted the fusion of the viral and late endosomal membranes,thereby facilitating IAV replication. Together, our findings highlight the importance of the M6PR–HA interaction in the fusion of viral and late endosomal membranes during IAV replication. | Yuzhen Hu Li Jiang Guangwen Wang Yangming Song Zhibo Shan Xuyuan Wang Guohua Deng Jianzhong Shi Guobin Tian Xianying Zeng Liling Liu Hualan Chen Chengjun Li | 2024 | Science China(Life Sciences)2024，67，3： | 0 |
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