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Stem-loop recognition by DDX17 facilitates miRNA processing and antiviral defense.
Ryan H Moy1, Brian S Cole2, Ari Yasunaga1
1Department of Microbiology, Penn Genome Frontiers Institute, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA 19104, USA.
Cell
|August 16, 2014
Summary
The DEAD-box helicase DDX17 restricts Rift Valley fever virus (RVFV) infection. This immune role is conserved and independent of interferon, involving DDX17 binding to viral RNA and host microRNA precursors.
Area of Science:
- Molecular Biology
- Virology
- Immunology
Background:
- DEAD-box helicases are crucial for RNA metabolism.
- Emerging evidence indicates their involvement in immune responses.
- Rift Valley fever virus (RVFV) poses significant health risks.
Purpose of the Study:
- To investigate the role of DEAD-box helicase DDX17 in immunity against RVFV.
- To determine if DDX17's function is conserved and interferon-independent.
Main Methods:
- RNA interference (RNAi) screening in Drosophila and human cells.
- Viral replication assays.
- Crosslinking immunoprecipitation high-throughput sequencing (CLIP-seq).
Main Results:
- Loss of DDX17 (Rm62 in Drosophila) enhanced RVFV infection.
- Depletion of human DDX17, but not DDX5, increased RVFV replication.
- DDX17 binds host pri-miRNA stem loops for processing and viral RNA stem loops to restrict infection.
Conclusions:
- DDX17 plays a conserved, interferon-independent role in restricting RVFV infection.
- DDX17 exhibits dual stem-loop recognition: facilitating host miRNA biogenesis and restricting viral RNA.
- DDX17 acts as a cytoplasmic sensor for structured viral RNA elements.
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