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mRNA expression and functional analysis of chicken IFIT5 after infected with Newcastle disease virus

Innate immunity is the first line against the invasion of pathogenic microorganisms. Over the past several years, the antiviral activity and mechanisms of the IFIT5 gene have been confirmed in mammals. However, more information is needed on the role of IFIT5 in response to viral infection in chicken...

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Published in:Infection, genetics and evolution genetics and evolution, 2020-12, Vol.86, p.104585-104585, Article 104585
Main Authors: Li, Jing-Jing, Yin, Yue, Yang, Hui-Lin, Yang, Chao-Wu, Yu, Chun-Lin, Wang, Yan, Yin, Hua-Dong, Lian, Ting, Peng, Han, Zhu, Qing, Liu, Yi-Ping
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Language:English
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Summary:Innate immunity is the first line against the invasion of pathogenic microorganisms. Over the past several years, the antiviral activity and mechanisms of the IFIT5 gene have been confirmed in mammals. However, more information is needed on the role of IFIT5 in response to viral infection in chickens. In this study, we examined the mRNA expression profile of chicken IFIT5 (chIFIT5) in different tissues and explored how chIFIT5 transduces upstream signaling to the downstream adaptor. Relative mRNA expression level of chIFIT5 was the highest in spleen and expression level of chIFIT5 was significantly up-regulated following Newcastle disease virus (NDV) infection, and polyinosinic:polycytidylic acid [poly (I:C)]- and poly(deoxyadenylic-thymidylic) [poly (dA:dT)]-triggered antiviral immune responses. Chicken MDA5, MAVS, and IRF7 positively regulated the mRNA expression of chIFIT5. Overexpression of chIFIT5 could promote IRF7- and NF-κB-mediated gene expression following NDV infection or transfection with poly (I:C). These results suggested that chIFIT5 is an important enhancer of the innate immunity response. •MDA5, MAVS, and IRF7 positively regulated mRNA expression of chIFIT5.•Overexpression of chIFIT5 promote IRF7- and NF-κB-mediated gene expression.•ChIFIT5 is an important enhancer of the innate immunity response.
ISSN:1567-1348
1567-7257
DOI:10.1016/j.meegid.2020.104585