HDAC6 Facilitates PRV and VSV Infection by Inhibiting Type I Interferon Production
HDAC6 modulates viral infection through diverse mechanisms. Here, we investigated the role of HDAC6 in influencing viral infection in pig cells with the aim of exploiting the potential antiviral gene targets in pigs. Using gene knockout and overexpression strategies, we found that HDAC6 knockout gre...
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| Format: | Article |
| Language: | English |
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MDPI AG
2025-01-01
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| Series: | Viruses |
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| Online Access: | https://www.mdpi.com/1999-4915/17/1/90 |
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| author | Hu Zheng Xiaohui Yang Haiwen Zhong Changxu Song Zhenfang Wu Huaqiang Yang |
| author_facet | Hu Zheng Xiaohui Yang Haiwen Zhong Changxu Song Zhenfang Wu Huaqiang Yang |
| author_sort | Hu Zheng |
| collection | DOAJ |
| description | HDAC6 modulates viral infection through diverse mechanisms. Here, we investigated the role of HDAC6 in influencing viral infection in pig cells with the aim of exploiting the potential antiviral gene targets in pigs. Using gene knockout and overexpression strategies, we found that HDAC6 knockout greatly reduced PRV and VSV infectivity, whereas HDAC6 overexpression increased their infectivity in PK15 cells. Mechanistic studies identified HDAC6 as a DNA damage inhibitor in PK15 cells. HDAC6 overexpression attenuated DNA damage levels, which can further reduce type I IFN production to promote viral infection. Conversely, HDAC6 deficiency can limit viral infection by increasing DNA damage-mediated type I IFN production. This work demonstrates that HDAC6 affects the infection process of multiple viruses by modulating type I IFN production, highlighting a regulatory role of HDAC6 linking host immune response and viral infection levels in pig cells. |
| format | Article |
| id | doaj-art-ae4f25f552304fa3bb4f9ff06e7380b8 |
| institution | Kabale University |
| issn | 1999-4915 |
| language | English |
| publishDate | 2025-01-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Viruses |
| spelling | doaj-art-ae4f25f552304fa3bb4f9ff06e7380b82025-01-24T13:52:33ZengMDPI AGViruses1999-49152025-01-011719010.3390/v17010090HDAC6 Facilitates PRV and VSV Infection by Inhibiting Type I Interferon ProductionHu Zheng0Xiaohui Yang1Haiwen Zhong2Changxu Song3Zhenfang Wu4Huaqiang Yang5State Key Laboratory of Swine and Poultry Breeding Industry, National Engineering Research Center for Breeding Swine Industry, College of Animal Science, South China Agricultural University, Guangzhou 510642, ChinaState Key Laboratory of Swine and Poultry Breeding Industry, National Engineering Research Center for Breeding Swine Industry, College of Animal Science, South China Agricultural University, Guangzhou 510642, ChinaState Key Laboratory of Swine and Poultry Breeding Industry, National Engineering Research Center for Breeding Swine Industry, College of Animal Science, South China Agricultural University, Guangzhou 510642, ChinaState Key Laboratory of Swine and Poultry Breeding Industry, National Engineering Research Center for Breeding Swine Industry, College of Animal Science, South China Agricultural University, Guangzhou 510642, ChinaState Key Laboratory of Swine and Poultry Breeding Industry, National Engineering Research Center for Breeding Swine Industry, College of Animal Science, South China Agricultural University, Guangzhou 510642, ChinaState Key Laboratory of Swine and Poultry Breeding Industry, National Engineering Research Center for Breeding Swine Industry, College of Animal Science, South China Agricultural University, Guangzhou 510642, ChinaHDAC6 modulates viral infection through diverse mechanisms. Here, we investigated the role of HDAC6 in influencing viral infection in pig cells with the aim of exploiting the potential antiviral gene targets in pigs. Using gene knockout and overexpression strategies, we found that HDAC6 knockout greatly reduced PRV and VSV infectivity, whereas HDAC6 overexpression increased their infectivity in PK15 cells. Mechanistic studies identified HDAC6 as a DNA damage inhibitor in PK15 cells. HDAC6 overexpression attenuated DNA damage levels, which can further reduce type I IFN production to promote viral infection. Conversely, HDAC6 deficiency can limit viral infection by increasing DNA damage-mediated type I IFN production. This work demonstrates that HDAC6 affects the infection process of multiple viruses by modulating type I IFN production, highlighting a regulatory role of HDAC6 linking host immune response and viral infection levels in pig cells.https://www.mdpi.com/1999-4915/17/1/90HDAC6PRVVSVType I IFNantiviral immunityhost-virus interaction |
| spellingShingle | Hu Zheng Xiaohui Yang Haiwen Zhong Changxu Song Zhenfang Wu Huaqiang Yang HDAC6 Facilitates PRV and VSV Infection by Inhibiting Type I Interferon Production Viruses HDAC6 PRV VSV Type I IFN antiviral immunity host-virus interaction |
| title | HDAC6 Facilitates PRV and VSV Infection by Inhibiting Type I Interferon Production |
| title_full | HDAC6 Facilitates PRV and VSV Infection by Inhibiting Type I Interferon Production |
| title_fullStr | HDAC6 Facilitates PRV and VSV Infection by Inhibiting Type I Interferon Production |
| title_full_unstemmed | HDAC6 Facilitates PRV and VSV Infection by Inhibiting Type I Interferon Production |
| title_short | HDAC6 Facilitates PRV and VSV Infection by Inhibiting Type I Interferon Production |
| title_sort | hdac6 facilitates prv and vsv infection by inhibiting type i interferon production |
| topic | HDAC6 PRV VSV Type I IFN antiviral immunity host-virus interaction |
| url | https://www.mdpi.com/1999-4915/17/1/90 |
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