PUBLICATION
Fish-specific finTRIM FTR36 triggers IFN pathway and mediates inhibition of viral replication
- Authors
- Chen, B., Huo, S., Liu, W., Wang, F., Lu, Y., Xu, Z., Liu, X.
- ID
- ZDB-PUB-190323-12
- Date
- 2019
- Source
- Fish & shellfish immunology 84: 876-884 (Journal)
- Registered Authors
- Keywords
- Antiviral, FTR36, Interferon, finTRIM
- MeSH Terms
-
- Animals
- Cell Line
- Cyprinidae
- DNA Virus Infections/immunology
- DNA Virus Infections/veterinary
- Fish Diseases/immunology*
- Fish Proteins/genetics*
- Fish Proteins/metabolism
- Interferons/genetics*
- Interferons/metabolism
- Ranavirus/physiology
- Rhabdoviridae/physiology
- Rhabdoviridae Infections/immunology
- Rhabdoviridae Infections/veterinary
- Virus Replication*
- Zebrafish
- PubMed
- 30366094 Full text @ Fish Shellfish Immunol.
Citation
Chen, B., Huo, S., Liu, W., Wang, F., Lu, Y., Xu, Z., Liu, X. (2019) Fish-specific finTRIM FTR36 triggers IFN pathway and mediates inhibition of viral replication. Fish & shellfish immunology. 84:876-884.
Abstract
The tripartite motif (TRIM) family involves many cellular processes, including fundamental functions in antiviral immunity. Antiviral activities of TRIMs are reported in a variety of patterns, and one of the most significant channels is related to the activation of the type-I interferon (IFN) pathway. In this study, we described a fintrim (ftr) gene named ftr36, which is mainly expressed in the gills, skin, and intestines. This study shows that ftr36 encodes a protein affording a potent antiviral effect. In vitro, overexpression of FTR36 mediated an upregulated pattern of recognition receptor retinoic acid-inducible gene I (RIG-I), interferon regulatory factor 3/7(IRF3/7), IFN, and IFN-stimulated genes (ISGs) expression. Thereby, FTR36 expression could afford host defense against the spring viremia of carp virus (SVCV) and the giant salamander iridovirus (GSIV). With the deletion of the RING domain or B30.2 domain separately, the antiviral ability of FTR36 was abolished partially and almost lost its ability to activate the IFN-pathway. These findings indicate that both RING and B30.2 domains are indispensable for the antiviral activity of FTR36. Altogether, this study described a finTRIM FTR36, which can activate IFN-pathways and stimulate ISGs to provide host defense against viral infections.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping