Tumor Necrosis Factor Receptor-Associated Factor 5 Interacts with the NS3 Protein and Promotes Classical Swine Fever Virus Replication
Classical swine fever, caused by classical swine fever virus (CSFV), is a highly contagious and high-mortality viral disease, causing huge economic losses in the swine industry worldwide. CSFV non-structural protein 3 (NS3), a multifunctional protein, plays crucial roles in viral replication. Howeve...
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| Format: | Article |
| Language: | English |
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MDPI AG
2018-06-01
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| Series: | Viruses |
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| Online Access: | http://www.mdpi.com/1999-4915/10/6/305 |
| _version_ | 1818343328851165184 |
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| author | Huifang Lv Wang Dong Kangkang Guo Mingxing Jin Xiaomeng Li Cunfa Li Yanming Zhang |
| author_facet | Huifang Lv Wang Dong Kangkang Guo Mingxing Jin Xiaomeng Li Cunfa Li Yanming Zhang |
| author_sort | Huifang Lv |
| collection | DOAJ |
| description | Classical swine fever, caused by classical swine fever virus (CSFV), is a highly contagious and high-mortality viral disease, causing huge economic losses in the swine industry worldwide. CSFV non-structural protein 3 (NS3), a multifunctional protein, plays crucial roles in viral replication. However, how NS3 exactly exerts these functions is currently unknown. Here, we identified tumor necrosis factor receptor-associated factor 5 (TRAF5) as a novel binding partner of the NS3 protein via yeast two-hybrid, co-immunoprecipitation and glutathione S-transferase pull-down assays. Furthermore, we observed that TRAF5 promoted CSFV replication in porcine alveolar macrophages (PAMs). Additionally, CSFV infection or NS3 expression upregulated TRAF5 expression, implying that CSFV may exploit TRAF5 via NS3 for better growth. Moreover, CSFV infection and TRAF5 expression activated p38 mitogen activated protein kinase (MAPK) activity, and inhibition of p38 MAPK activation by the SB203580 inhibitor suppressed CSFV replication. Notably, TRAF5 overexpression did not promote CSFV replication following inhibition of p38 MAPK activation. Our findings reveal that TRAF5 promotes CSFV replication via p38 MAPK activation. This work provides a novel insight into the role of TRAF5 in CSFV replication capacity. |
| first_indexed | 2024-12-13T16:28:51Z |
| format | Article |
| id | doaj.art-754943f489ec4582a70974fcdb94f9ab |
| institution | Directory Open Access Journal |
| issn | 1999-4915 |
| language | English |
| last_indexed | 2024-12-13T16:28:51Z |
| publishDate | 2018-06-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Viruses |
| spelling | doaj.art-754943f489ec4582a70974fcdb94f9ab2022-12-21T23:38:33ZengMDPI AGViruses1999-49152018-06-0110630510.3390/v10060305v10060305Tumor Necrosis Factor Receptor-Associated Factor 5 Interacts with the NS3 Protein and Promotes Classical Swine Fever Virus ReplicationHuifang Lv0Wang Dong1Kangkang Guo2Mingxing Jin3Xiaomeng Li4Cunfa Li5Yanming Zhang6College of Veterinary Medicine, Northwest A&F University, Yangling 712100, ChinaCollege of Veterinary Medicine, Northwest A&F University, Yangling 712100, ChinaCollege of Veterinary Medicine, Northwest A&F University, Yangling 712100, ChinaCollege of Veterinary Medicine, Northwest A&F University, Yangling 712100, ChinaNingbo Entry-Exit Inspection and Quarantine Bureau, Ningbo 315000, ChinaCollege of Pharmaceutical Engineering, Henan University of Animal Husbandry and Economy, Zhengzhou 450046, ChinaCollege of Veterinary Medicine, Northwest A&F University, Yangling 712100, ChinaClassical swine fever, caused by classical swine fever virus (CSFV), is a highly contagious and high-mortality viral disease, causing huge economic losses in the swine industry worldwide. CSFV non-structural protein 3 (NS3), a multifunctional protein, plays crucial roles in viral replication. However, how NS3 exactly exerts these functions is currently unknown. Here, we identified tumor necrosis factor receptor-associated factor 5 (TRAF5) as a novel binding partner of the NS3 protein via yeast two-hybrid, co-immunoprecipitation and glutathione S-transferase pull-down assays. Furthermore, we observed that TRAF5 promoted CSFV replication in porcine alveolar macrophages (PAMs). Additionally, CSFV infection or NS3 expression upregulated TRAF5 expression, implying that CSFV may exploit TRAF5 via NS3 for better growth. Moreover, CSFV infection and TRAF5 expression activated p38 mitogen activated protein kinase (MAPK) activity, and inhibition of p38 MAPK activation by the SB203580 inhibitor suppressed CSFV replication. Notably, TRAF5 overexpression did not promote CSFV replication following inhibition of p38 MAPK activation. Our findings reveal that TRAF5 promotes CSFV replication via p38 MAPK activation. This work provides a novel insight into the role of TRAF5 in CSFV replication capacity.http://www.mdpi.com/1999-4915/10/6/305CSFVNS3p38 MAPKTRAF5replication |
| spellingShingle | Huifang Lv Wang Dong Kangkang Guo Mingxing Jin Xiaomeng Li Cunfa Li Yanming Zhang Tumor Necrosis Factor Receptor-Associated Factor 5 Interacts with the NS3 Protein and Promotes Classical Swine Fever Virus Replication Viruses CSFV NS3 p38 MAPK TRAF5 replication |
| title | Tumor Necrosis Factor Receptor-Associated Factor 5 Interacts with the NS3 Protein and Promotes Classical Swine Fever Virus Replication |
| title_full | Tumor Necrosis Factor Receptor-Associated Factor 5 Interacts with the NS3 Protein and Promotes Classical Swine Fever Virus Replication |
| title_fullStr | Tumor Necrosis Factor Receptor-Associated Factor 5 Interacts with the NS3 Protein and Promotes Classical Swine Fever Virus Replication |
| title_full_unstemmed | Tumor Necrosis Factor Receptor-Associated Factor 5 Interacts with the NS3 Protein and Promotes Classical Swine Fever Virus Replication |
| title_short | Tumor Necrosis Factor Receptor-Associated Factor 5 Interacts with the NS3 Protein and Promotes Classical Swine Fever Virus Replication |
| title_sort | tumor necrosis factor receptor associated factor 5 interacts with the ns3 protein and promotes classical swine fever virus replication |
| topic | CSFV NS3 p38 MAPK TRAF5 replication |
| url | http://www.mdpi.com/1999-4915/10/6/305 |
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