Duck Tembusu Virus Infection Promotes the Expression of Duck Interferon-Induced Protein 35 to Counteract RIG-I Antiviral Signaling in Duck Embryo Fibroblasts
| Autor: | Peng Zhou, Lei Ma, Zaixiao Rao, Yaqian Li, Huijun Zheng, Qigai He, Rui Luo |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2021 |
| Předmět: |
0301 basic medicine
Gene Expression Regulation Viral Proteomics medicine.drug_class duck Tembusu virus 030106 microbiology Immunology Biology interferon-induced protein 35 Cell Line Flavivirus Infections RIG-I 03 medical and health sciences Interferon Genes Reporter Tandem Mass Spectrometry Stable isotope labeling by amino acids in cell culture medicine Immunology and Allergy Animals Humans RNA Small Interfering Poultry Diseases Original Research Immune Evasion RNA Double-Stranded Innate immune system Flavivirus Intracellular Signaling Peptides and Proteins quantitative proteomic analysis MDA5 interferon Interferon-beta RC581-607 Fibroblasts Virology 030104 developmental biology Ducks HEK293 Cells Poly I-C Viral replication IRF7 RNA Interference Immunologic diseases. Allergy Antiviral drug medicine.drug Signal Transduction |
| Zdroj: | Frontiers in Immunology Frontiers in Immunology, Vol 12 (2021) |
| ISSN: | 1664-3224 |
| Popis: | Duck Tembusu virus (DTMUV) is an emerging pathogenic flavivirus that has caused a substantial drop in egg production and severe neurological disorders in domestic waterfowl. Several studies have revealed that viral proteins encoded by DTMUV antagonize host IFN-mediated antiviral responses to facilitate virus replication. However, the role of host gene expression regulated by DTMUV in innate immune evasion remains largely unknown. Here, we utilized a stable isotope labeling with amino acids in cell culture (SILAC)-based proteomics analysis of DTMUV-infected duck embryo fibroblasts (DEFs) to comprehensively investigate host proteins involved in DTMUV replication and innate immune response. A total of 250 differentially expressed proteins were identified from 2697 quantified cellular proteins, among which duck interferon-induced protein 35 (duIFI35) was dramatically up-regulated due to DTMUV infection in DEFs. Next, we demonstrated that duIFI35 expression promoted DTMUV replication and impaired Sendai virus-induced IFN-β production. Moreover, duIFI35 was able to impede duck RIG-I (duRIG-I)-induced IFN-β promoter activity, rather than IFN-β transcription mediated by MDA5, MAVS, TBK1, IKKϵ, and IRF7. Importantly, we found that because of the specific interaction with duIFI35, the capacity of duRIG-I to recognize double-stranded RNA was significantly impaired, resulting in the decline of duRIG-I-induced IFN-β production. Taken together, our data revealed that duIFI35 expression stimulated by DTMUV infection disrupted duRIG-I-mediated host antiviral response, elucidating a distinct function of duIFI35 from human IFI35, by which DTMUV escapes host innate immune response, and providing information for the design of antiviral drug. |
| Databáze: | OpenAIRE |
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