The role of IBV PL1pro in virus replication and suppression of host innate immune responses
Abstract Background Coronavirus papain-like proteases (PLpros) play a crucial role in virus replication and the evasion of the host immune response. Infectious bronchitis virus (IBV) encodes a proteolytically defective remnant of PL1pro and an active PL2pro. However, the function of PL1pro in IBV re...
Main Authors: | , , , , , , |
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Language: | English |
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BMC
2023-12-01
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Series: | BMC Veterinary Research |
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Online Access: | https://doi.org/10.1186/s12917-023-03839-2 |
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author | Weirong Liu Ge Mu Yiquan Jia Mengting Yu Songbai Zhang Zhen Wang Shouguo Fang |
author_facet | Weirong Liu Ge Mu Yiquan Jia Mengting Yu Songbai Zhang Zhen Wang Shouguo Fang |
author_sort | Weirong Liu |
collection | DOAJ |
description | Abstract Background Coronavirus papain-like proteases (PLpros) play a crucial role in virus replication and the evasion of the host immune response. Infectious bronchitis virus (IBV) encodes a proteolytically defective remnant of PL1pro and an active PL2pro. However, the function of PL1pro in IBV remains largely unknown. This study aims to explore the effect of PL1pro on virus replication and underlying mechanisms. Results The recombinant viruses rIBV-ΔPL1pro and rIBV-ΔPL1pro-N were obtained using reverse genetic techniques through the deletion of the IBV PL1pro domain and the N-terminal conserved sequence of PL1pro (PL1pro-N). We observed significantly lower replication of rIBV-ΔPL1pro and rIBV-ΔPL1pro-N than wild-type IBV. Further investigation revealed that the lack of PL1pro-N in IBV decreased virus resistance to interferon (IFN) while also inducing host immune response by enhancing the production of IFN-β and activating the downstream STAT1 signaling pathway of IFNs. In addition, the overexpression of PL1pro-N significantly suppressed type I IFN response by down-regulating the expressions of genes in the IFN pathway. Conclusions Our data demonstrated that IBV PL1pro plays a crucial role in IBV replication and the suppression of host innate immune responses, suggesting that IBV PL1pro could serve as a promising molecular target for antiviral therapy. |
first_indexed | 2024-03-08T22:38:56Z |
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id | doaj.art-f8529ac6f0864ba7ba8165583101b5e0 |
institution | Directory Open Access Journal |
issn | 1746-6148 |
language | English |
last_indexed | 2024-03-08T22:38:56Z |
publishDate | 2023-12-01 |
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series | BMC Veterinary Research |
spelling | doaj.art-f8529ac6f0864ba7ba8165583101b5e02023-12-17T12:20:36ZengBMCBMC Veterinary Research1746-61482023-12-0119111510.1186/s12917-023-03839-2The role of IBV PL1pro in virus replication and suppression of host innate immune responsesWeirong Liu0Ge Mu1Yiquan Jia2Mengting Yu3Songbai Zhang4Zhen Wang5Shouguo Fang6Yangtze University Health Science CenterCollege of Agriculture, Yangtze UniversityCollege of Agriculture, Yangtze UniversityCollege of Agriculture, Yangtze UniversityMARA Key Laboratory of Sustainable Crop Production in the Middle Reaches of the Yangtze River (Co-construction by Ministry and Province), College of Agriculture, Yangtze UniversityYangtze University Health Science CenterCollege of Agriculture, Yangtze UniversityAbstract Background Coronavirus papain-like proteases (PLpros) play a crucial role in virus replication and the evasion of the host immune response. Infectious bronchitis virus (IBV) encodes a proteolytically defective remnant of PL1pro and an active PL2pro. However, the function of PL1pro in IBV remains largely unknown. This study aims to explore the effect of PL1pro on virus replication and underlying mechanisms. Results The recombinant viruses rIBV-ΔPL1pro and rIBV-ΔPL1pro-N were obtained using reverse genetic techniques through the deletion of the IBV PL1pro domain and the N-terminal conserved sequence of PL1pro (PL1pro-N). We observed significantly lower replication of rIBV-ΔPL1pro and rIBV-ΔPL1pro-N than wild-type IBV. Further investigation revealed that the lack of PL1pro-N in IBV decreased virus resistance to interferon (IFN) while also inducing host immune response by enhancing the production of IFN-β and activating the downstream STAT1 signaling pathway of IFNs. In addition, the overexpression of PL1pro-N significantly suppressed type I IFN response by down-regulating the expressions of genes in the IFN pathway. Conclusions Our data demonstrated that IBV PL1pro plays a crucial role in IBV replication and the suppression of host innate immune responses, suggesting that IBV PL1pro could serve as a promising molecular target for antiviral therapy.https://doi.org/10.1186/s12917-023-03839-2Infectious Bronchitis virusPapain-like proteaseVirus replicationInterferonImmune response |
spellingShingle | Weirong Liu Ge Mu Yiquan Jia Mengting Yu Songbai Zhang Zhen Wang Shouguo Fang The role of IBV PL1pro in virus replication and suppression of host innate immune responses BMC Veterinary Research Infectious Bronchitis virus Papain-like protease Virus replication Interferon Immune response |
title | The role of IBV PL1pro in virus replication and suppression of host innate immune responses |
title_full | The role of IBV PL1pro in virus replication and suppression of host innate immune responses |
title_fullStr | The role of IBV PL1pro in virus replication and suppression of host innate immune responses |
title_full_unstemmed | The role of IBV PL1pro in virus replication and suppression of host innate immune responses |
title_short | The role of IBV PL1pro in virus replication and suppression of host innate immune responses |
title_sort | role of ibv pl1pro in virus replication and suppression of host innate immune responses |
topic | Infectious Bronchitis virus Papain-like protease Virus replication Interferon Immune response |
url | https://doi.org/10.1186/s12917-023-03839-2 |
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