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Your search keyword '"Meng, Lingzhai"' showing total 8 results
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8 results on '"Meng, Lingzhai"'

2. Development of an improved reverse genetics system for avian metapneumovirus (aMPV): A novel vaccine vector protects against aMPV and infectious bursal disease virus

Author

Meng, Lingzhai, primary, Chen, Yuntong, additional, Yu, Mengmeng, additional, Liu, Peng, additional, Qi, Xiaole, additional, Xue, Xiaoxiao, additional, Guo, Ru, additional, Zhang, Tao, additional, Hu, Mingxue, additional, Fan, Wenrui, additional, Wang, Ying, additional, Wang, Suyan, additional, Zhang, Yanping, additional, Liu, Yongzhen, additional, Duan, Yulu, additional, Cui, Hongyu, additional, and Gao, Yulong, additional

Published
2024
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3. N123I mutation in the ALV-J receptor-binding domain region enhances viral replication ability by increasing the binding affinity with chNHE1

Author

Yu, Mengmeng, primary, Zhang, Yao, additional, Zhang, Li, additional, Wang, Suyan, additional, Liu, Yongzhen, additional, Xu, Zhuangzhuang, additional, Liu, Peng, additional, Chen, Yuntong, additional, Guo, Ru, additional, Meng, Lingzhai, additional, Zhang, Tao, additional, Fan, Wenrui, additional, Qi, Xiaole, additional, Gao, Li, additional, Zhang, Yanping, additional, Cui, Hongyu, additional, and Gao, Yulong, additional

Published
2024
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4. Residues E53, L55, H59, and G70 of the cellular receptor protein Tva mediate cell binding and entry of the novel subgroup K avian leukosis virus

Author

Li, Xinyi, primary, Chen, Yuntong, additional, Yu, Mengmeng, additional, Wang, Suyan, additional, Liu, Peng, additional, Meng, Lingzhai, additional, Guo, Ru, additional, Feng, Xiaoyan, additional, Hu, Mingxue, additional, He, Tana, additional, Qi, Xiaole, additional, Li, Kai, additional, Gao, Li, additional, Zhang, Yanping, additional, Liu, Changjun, additional, Cui, Hongyu, additional, Wang, Xiaomei, additional, and Gao, Yulong, additional

Published
2023
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5. Residues L55 and W69 of Tva Mediate Entry of Subgroup A Avian Leukosis Virus

Author

Chen, Yuntong, primary, Wang, Suyan, additional, Li, Xinyi, additional, Yu, Mengmeng, additional, Liu, Peng, additional, Meng, Lingzhai, additional, Guo, Ru, additional, Feng, Xiaoyan, additional, Liu, Aijing, additional, Qi, Xiaole, additional, Li, Kai, additional, Gao, Li, additional, Pan, Qing, additional, Zhang, Yanping, additional, Liu, Changjun, additional, Cui, Hongyu, additional, Wang, Xiaomei, additional, and Gao, Yulong, additional

Published
2022
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6. TRIM25 inhibits infectious bursal disease virus replication by targeting VP3 for ubiquitination and degradation

Author

Wang, Suyan, primary, Yu, Mengmeng, additional, Liu, Aijing, additional, Bao, Yuanling, additional, Qi, Xiaole, additional, Gao, Li, additional, Chen, Yuntong, additional, Liu, Peng, additional, Wang, Yulong, additional, Xing, Lixiao, additional, Meng, Lingzhai, additional, Zhang, Yu, additional, Fan, Linjin, additional, Li, Xinyi, additional, Pan, Qing, additional, Zhang, Yanping, additional, Cui, Hongyu, additional, Li, Kai, additional, Liu, Changjun, additional, He, Xijun, additional, Gao, Yulong, additional, and Wang, Xiaomei, additional

Published
2021
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8. OASL suppresses infectious bursal disease virus replication by targeting VP2 for degrading through the autophagy pathway.

Author

Wang S, Xu Z, Liu Y, Yu M, Zhang T, Liu P, Qi X, Chen Y, Meng L, Guo R, Zhang L, Fan W, Gao L, Duan Y, Zhang Y, Cui H, and Gao Y

Subjects
Animals, Poultry Diseases virology, Poultry Diseases metabolism, Host-Pathogen Interactions, HEK293 Cells, Humans, Cell Line, Infectious bursal disease virus physiology, Virus Replication, Autophagy, Birnaviridae Infections virology, Birnaviridae Infections metabolism, Viral Structural Proteins metabolism, Viral Structural Proteins genetics, Chickens, 2',5'-Oligoadenylate Synthetase metabolism, 2',5'-Oligoadenylate Synthetase genetics
Abstract

Infectious bursal disease (IBD) is an acute and fatal immunosuppressive disease caused by infectious bursal disease virus (IBDV). As an obligate intracellular parasite, IBDV infection is strictly regulated by host factors. Knowledge on the antiviral activity and possible mechanism of host factors might provide the theoretical basis for the prevention and control of IBD. In this study, RNA-sequencing results indicated that many host factors were induced by IBDV infection, among which the expression levels of OASL (2´,5´-oligadenylate synthetase-like protein) was significantly upregulated. OASL overexpression significantly inhibited IBDV replication, whereas OASL knockdown promoted IBDV replication. Interestingly, the antiviral ability of OASL was independent of its canonical enzymatic activity, i.e., OASL targeted viral protein VP2 for degradation, depending on the autophagy receptor p62/SQSTM1 in the autophagy pathway. Additionally, the 316 lysine (K) of VP2 was the key site for autophagy degradation, and its replacement with arginine disrupted VP2 degradation induced by OASL and enhanced IBDV replication. Importantly, our results for the first time indicate a unique and potent defense mechanism of OASL against double-stranded RNA virus by interaction with viral proteins, which leads to their degradation., Importance: OASL (2´,5´-oligadenylate synthetase-like protein) exhibits broad-spectrum antiviral effects against single-stranded RNA viruses in mammals, potentially serving as a promising target for novel antiviral strategies. However, its role in inhibiting the replication of double-stranded RNA viruses (dsRNA viruses), such as infectious bursal disease virus (IBDV), in avian species remains unclear. Our findings indicated a unique and potent defense mechanism of OASL against dsRNA viruses. It has been previously shown in mammals that OASL inhibits virus replication through increasing interferon production. The groundbreaking aspect of our study is the finding that OASL has the ability to interact with IBDV viral protein VP2 and target it for degradation and thus exerts its antiviral effect. Our results reveal the interaction between avian natural antiviral immune response and IBDV infection. Our study not only enhances our understanding of bird defenses against viral infections but can also inform strategies for poultry disease management., Competing Interests: The authors declare no conflict of interest.

Published
2024
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