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Inhibition of MAVS Signaling by PB1-F2 from H5N1 Highly Pathogenic Avian Influenza Viruses in Avian Cells

2021 CPRF,Gut Health, Antibiotic Alternatives & Management
Upon detection of viral RNA, RIG-I engages the critical adaptor protein mitochondrial antiviral signalling (MAVS) to activate the downstream signalling pathway, leading to Type I interferon production. The influenza A virus non-structural protein, PB1-F2, interacts with MAVS in human cells to inhibit interferon production. We have shown in previous experiments that PB1-F2 from influenza virus A/Puerto Rico/8/1934 (H1N1) (PR8) will inhibit interferon production in avian cells. However, it is not known if this is true for highly pathogenic avian influenza A strains. In 2004, two highly pathogenic strains of H5N1 emerged in Southeast Asia; A/duck/D4AT/2004 (D4AT) and A/Vietnam/1203/04 (VN1203). These strains differ in virulence due to differences in PB1-F2 sequences. Here we use a Dual-Luciferase® Reporter Assay to show that PB1-F2 from highly virulent avian influenza A strains, as well as a reverse-genetics recombinant of VN1203 (rgVN1203), significantly inhibit production of IFN-β in chicken cells (DF-1). Using confocal microscopy, we show that PB1-F2 from H5N1 strains co-localize with duck MAVS. We also showed by Western Blot that PB1-F2 is immunoprecipitated by duck MAVS. This research highlights the mechanism by which PB1-F2 inhibits host immunity across various human and avian influenza strains, and provides a possible anti-viral therapeutic target.
Tags :
avian influenza,virus detection
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MSc Student

University of Alberta

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