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Comparative analysis of selected innate immune-related genes following infection of immortal DF-1 cells with highly pathogenic (H5N1) and low pathogenic (H9N2) avian influenza viruses

文献类型： 外文期刊

作者： Liu, Ai-ling 1 ; Li, Yu-feng 2 ; Qi, Wenbao 3 ; Ma, Xiu-Li 2 ; Yu, Ke-xiang 2 ; Huang, Bing 2 ; Liao, Ming 3 ; Li, Feng 4 ;

作者机构： 1.Shandong Normal Univ, Key Lab Anim Resistance Biol Shandong, Coll Life Sci, Jinan 250014, Shandong, Peoples R China

2.Shandong Acad Agr Sci, Inst Poultry Sci, Jinan 250023, Shandong, Peoples R China

3.South China Agr Univ, Coll Vet Med, Guangzhou 510642, Guangdong, Peoples R China

4.S Dakota State Univ, Dept Vet & Biomed Sci, Brookings, SD 57007 USA

5.S Dakota State Univ, Dept Biol & Microbiol, Brookings, SD 57007 USA

关键词： H5N1;H9N2;Innate immune-related genes;Real-time quantitative PCR;Subtype-dependent host response

期刊名称：VIRUS GENES （ 影响因子：2.332； 五年影响因子：2.0 ）

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收录情况： SCI

摘要： H5N1 and H9N2 viruses are important causes of avian influenza in China. H5N1 is typically associated with severe to fatal disease in poultry, while H9N2 is usually associated with mild disease. Differences in viral virulence prompted us to investigate whether innate immune responses would be differentially regulated following infection by H5N1 and H9N2 viruses. To address this hypothesis, expression of a panel of innate immune-related genes including IFN-alpha, IFN-beta, Mx1, OASL, ISG12, IFIT5, IRF7, USP18, SST, and KHSRP in immortal DF-1 cells following H5N1 and H9N2 infection was analyzed and compared by real-time quantitative RT-PCR. Cells infected by either virus overall exhibited a similar expression profile for four ISGs (Mx1, OASL, ISG12, and IFIT5), IFN-alpha, IFN-beta, and SST gene. However, two immune-regulatory genes (IRF7 and KHSRP) were not responsive to highly pathogenic H5N1 infection but were strongly up-regulated in DF-1 cells infected with low pathogenic H9N2 infection. The subtype-dependent host response observed in this study offers new insights into the potential roles of IRF7 and KHSRP in control and modulation of the replication and virulence of different subtypes or strains of avian influenza A virus.

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