4.2 Article

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

Journal

VIRUS GENES
Volume 50, Issue 2, Pages 189-199

Publisher

SPRINGER
DOI: 10.1007/s11262-014-1151-z

Keywords

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

Funding

  1. International Science & Technology Cooperation Program of China - Shandong Modern Agricultural Technology & Industry System [2014DFA31900, SDAIT-13-011-01]
  2. Special fund for Agro-scientific research in the public interest [201303046-06]
  3. Innovation Project of Shandong Academy of Agricultural Sciences [2014CXZ08]
  4. Taishan Scholar Program

Ask authors/readers for more resources

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.

Authors

I am an author on this paper
Click your name to claim this paper and add it to your profile.

Reviews

Primary Rating

4.2
Not enough ratings

Secondary Ratings

Novelty
-
Significance
-
Scientific rigor
-
Rate this paper

Recommended

No Data Available
No Data Available