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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
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Zebrafish NF-κB/p65 Is Required for Antiviral Responses
Gang Ouyang1,2,3,4,5, Qian Liao1,2,3,4,5, Dawei Zhang1,2,3,4,5
1State Key Laboratory of Freshwater Ecology and Biotechnology, Institute of Hydrobiology, Chinese Academy of Sciences, Wuhan 430072, China.
Journal of Immunology (Baltimore, Md. : 1950)
|April 24, 2020
Summary
The transcription factor p65 (also known as NF-κB subunit p65) is crucial for antiviral immunity. Zebrafish lacking p65 showed increased susceptibility to viral infections, with reduced inflammatory and interferon gene expression.
Area of Science:
- Immunology
- Molecular Biology
- Virology
Background:
- Nuclear factor kappa B (NF-κB) signaling pathways regulate immune responses.
- The canonical NF-κB pathway, involving p65, is critical for immunity but its role in antiviral responses is unclear due to embryonic lethality in mice.
- Zebrafish offer a viable model to study p65's function in vivo.
Purpose of the Study:
- To investigate the physiological role of p65 in the antiviral immune response using a zebrafish model.
- To determine if p65 is essential for regulating genes involved in antiviral defense.
Main Methods:
- Generation of p65-null zebrafish.
- Infection of zebrafish with spring viremia of carp virus.
- Quantitative analysis of proinflammatory and antiviral gene expression (including Interferon/IFN) in p65-null and wildtype zebrafish.
Main Results:
- p65-null zebrafish were viable and phenotypically normal under standard conditions.
- p65-null zebrafish exhibited increased sensitivity to spring viremia of carp virus infection compared to wildtype siblings.
- Downregulation of key proinflammatory and antiviral genes, including Interferon (IFN), was observed in p65-null zebrafish post-infection.
Conclusions:
- p65 is essential for an effective antiviral immune response in zebrafish.
- p65 regulates the expression of both proinflammatory and antiviral genes, including Interferon (IFN), during viral infection.

