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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
[Influenza A virus-induced expression of ZFAS1 is regulated by type Ⅰ interferon and significantly suppresses the
Xiaojuan Chi1,2, Guiying Huang2, Jingjie Hong1
1Key Laboratory of Animal Pathogen Infection and Immunology of Fujian Province, College of Animal Sciences, Fujian Agriculture and Forestry University, Fuzhou 350002, Fujian, China.
Abstract:
To investigate the roles of long non-coding RNAs (lncRNAs) and potential micropeptides encoded by these lncRNAs in influenza A virus (IAV) replication, we analyzed the data obtained from RNA-seq and Ribo-seq. We found that the lncRNA zinc finger antisense 1 (ZFAS1) was significantly up-regulated by IAV infection. This finding was confirmed by in vitro experiments, which showed that IAV infection caused a significant increase in the expression of ZFAS1, with the effect exhibiting a dose- and time-dependent relationship in response to the viral infection. This up-regulation was also observed in cells infected with other RNA and DNA viruses. Furthermore, we discovered that the type Ⅰ interferon signaling pathway positively regulated ZFAS1 expression. Functional assays revealed that silencing ZFAS1 significantly promoted IAV replication, while its overexpression significantly suppressed the virus replication. Additionally, LC-MS/MS analysis and Western blotting suggested that ZFAS1 encoded a 56-aa micropeptide, named ZFAS1-P56, which can also inhibit IAV replication. These results reveal that IAV-induced expression of ZFAS1 is regulated via the type Ⅰ interferon signaling pathway, and both ZFAS1 and ZFAS1-P56 suppress the IAV replication. This study unveils a new mechanism by which host establishes an innate immunity against the viral infection.
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