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Using Zebrafish Models of Human Influenza A Virus Infections to Screen Antiviral Drugs and Characterize Host Immune Cell Responses
Published on: January 20, 2017
Zebrafish prmt3 negatively regulates antiviral responses
Junji Zhu1,2, Xing Liu1,3,4, Xiaolian Cai1,2
1State Key Laboratory of Freshwater Ecology and Biotechnology, Institute of Hydrobiology, Chinese Academy of Sciences, Wuhan, P.R. China.
Protein arginine methyltransferase 3 (PRMT3) negatively regulates the antiviral innate immune response. Inhibiting PRMT3 or creating PRMT3-null zebrafish enhances resistance to viral infections, suggesting arginine methylation
Area of Science:
- Biochemistry
- Immunology
- Molecular Biology
Background:
- Arginine methylation is a crucial post-translational modification regulating protein function.
- Protein arginine methyltransferase 3 (PRMT3) is involved in methylation, but its role in antiviral immunity is unknown.
Purpose of the Study:
- To investigate the role of PRMT3 in the innate immune response to viral infections in zebrafish.
Main Methods:
- Zebrafish models were used to study PRMT3 expression and function during viral infections.
- PRMT3 inhibitors (SGC707) and PRMT3-null zebrafish were employed.
- Interactions with key antiviral signaling molecules like IRF3 and RIG-I were analyzed.
Main Results:
- Zebrafish prmt3 expression increased upon viral infection.
- Overexpression of prmt3 suppressed antiviral responses, while its inhibition or absence enhanced resistance to viruses (SVCV, GCRV).
- PRMT3 negatively impacted IRF3 phosphorylation and interacted with RIG-I, with both zinc-finger and catalytic domains being essential for its suppressive function on IFN activation.
Conclusions:
- Zebrafish PRMT3 acts as a negative regulator of the antiviral innate immune response.
- PRMT3 and potentially arginine methylation play a significant role in modulating antiviral immunity.
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