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Histone deacetylase 8 promotes innate antiviral immunity through deacetylation of RIG-I.
- Source :
-
Frontiers in cellular and infection microbiology [Front Cell Infect Microbiol] 2024 Jul 05; Vol. 14, pp. 1415695. Date of Electronic Publication: 2024 Jul 05 (Print Publication: 2024). - Publication Year :
- 2024
-
Abstract
- Histone deacetylates family proteins have been studied for their function in regulating viral replication by deacetylating non-histone proteins. RIG-I (Retinoic acid-inducible gene I) is a critical protein in RNA virus-induced innate antiviral signaling pathways. Our previous research showed that HDAC8 (histone deacetylase 8) involved in innate antiviral immune response, but the underlying mechanism during virus infection is still unclear. In this study, we showed that HDAC8 was involved in the regulation of vesicular stomatitis virus (VSV) replication. Over-expression of HDAC8 inhibited while knockdown promoted VSV replication. Further exploration demonstrated that HDAC8 interacted with and deacetylated RIG-I, which eventually lead to enhance innate antiviral immune response. Collectively, our data clearly demonstrated that HDAC8 inhibited VSV replication by promoting RIG-I mediated interferon production and downstream signaling pathway.<br />Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.<br /> (Copyright © 2024 Zhang, Liu, Liu, You, Yang, Zhang, Huang and Liang.)
- Subjects :
- Humans
Repressor Proteins metabolism
Repressor Proteins genetics
Acetylation
HEK293 Cells
Interferons metabolism
Interferons immunology
Cell Line
Host-Pathogen Interactions immunology
Animals
Vesicular stomatitis Indiana virus immunology
DEAD Box Protein 58 metabolism
DEAD Box Protein 58 genetics
Immunity, Innate
Histone Deacetylases metabolism
Virus Replication
Vesiculovirus immunology
Signal Transduction
Receptors, Immunologic metabolism
Subjects
Details
- Language :
- English
- ISSN :
- 2235-2988
- Volume :
- 14
- Database :
- MEDLINE
- Journal :
- Frontiers in cellular and infection microbiology
- Publication Type :
- Academic Journal
- Accession number :
- 39035358
- Full Text :
- https://doi.org/10.3389/fcimb.2024.1415695