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Influenza PB1-F2 Inhibits Avian MAVS Signaling.
Yanna Xiao1,2, Danyel Evseev2,3, Chase A Stevens2
1Department of Medical Microbiology and Immunology, University of Alberta, Edmonton, AB T6G 2R3, Canada.
Viruses
|April 11, 2020
Summary
Duck RIG-I (retinoic acid-inducible gene I) protein interacts with MAVS to trigger innate immunity. Influenza PB1-F2 protein inhibits this pathway in ducks, impacting interferon production and viral defense.
Area of Science:
- Immunology
- Virology
- Molecular Biology
Background:
- RIG-I (retinoic acid-inducible gene I) is crucial for duck innate immunity against influenza.
- MAVS (mitochondrial antiviral signaling) is an adaptor protein that activates downstream signaling pathways.
- Influenza A virus PB1-F2 protein inhibits interferon production by interacting with MAVS in human cells.
Purpose of the Study:
- To investigate if influenza virus PB1-F2 can inhibit MAVS signaling in avian cells.
- To explore the cross-species interaction of RIG-I and MAVS between avian and human cells.
- To determine the mechanism by which PB1-F2 inhibits RIG-I/MAVS signaling.
Main Methods:
- Confocal microscopy to visualize protein co-localization.
- Co-immunoprecipitation to confirm protein interactions.
- Reporter assays to measure interferon-beta promoter activity.
Main Results:
- Duck RIG-I and MAVS co-localize and interact in chicken DF-1 cells.
- Duck RIG-I activates MAVS signaling in chicken cells but poorly in human cells.
- Influenza PB1-F2 localizes to mitochondria, interacts with duck MAVS, and inhibits interferon-beta promoter activity.
- PB1-F2 abrogates RIG-I ubiquitination, hindering innate immune signaling.
Conclusions:
- Duck MAVS signaling can be inhibited by influenza PB1-F2 in avian cells.
- Cross-species RIG-I/MAVS interactions are limited, with specific mutations affecting signaling.
- PB1-F2 disrupts the RIG-I innate immune pathway by interfering with MAVS and ubiquitination.
