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SMARCA2-regulated host cell factors are required for MxA restriction of influenza A viruses

Dominik Dornfeld1,2, Alexandra H Dudek1,3,2,4, Thibaut Vausselin5

  • 1Institute of Virology, Medical Center, University of Freiburg, 79104, Freiburg, Germany.

Scientific Reports
|February 3, 2018
PubMed

Insights

The MxA protein restricts influenza A virus (IAV) but needs help. Researchers found SMARCA2 and factors like IFITM2 are crucial for MxA

Area of Science:

  • Virology
  • Immunology
  • Cell Biology

Background:

  • The MxA protein is a crucial host factor against RNA viruses, including avian influenza A viruses (IAV).
  • The precise mechanism of MxA antiviral activity and its required cofactors remain largely unknown.
  • Identifying cellular factors interacting with MxA is essential to understand its broad antiviral function.

Purpose of the Study:

  • To identify cellular cofactors essential for the antiviral activity of the human interferon (IFN)-induced MxA protein against IAV.
  • To elucidate the mechanism by which MxA restricts IAV replication in host cells.
  • To uncover the interplay between MxA and other IFN-stimulated genes (ISGs) in antiviral defense.

Main Methods:

  • Genome-wide siRNA screening in A549 cells expressing MxA using an H5N1 reporter virus.
  • Proteomic analysis to identify proteins interacting with MxA.
  • Transcriptome analysis of cells depleted of SMARCA2 to identify key factors for MxA activity.

Main Results:

  • SMARCA2, a subunit of the BAF chromatin remodeling complex, was identified as essential for MxA's antiviral activity against IAV.
  • SMARCA2 is not required for MxA expression but influences its activity indirectly.
  • IFITM2 and IGFBP3 were identified as key SMARCA2-regulated factors necessary for MxA-mediated IAV restriction.

Conclusions:

  • SMARCA2 plays a critical, indirect role in enabling MxA's antiviral function against IAV.
  • MxA antiviral activity is dependent on a network of virus-inducible factors, including IFITM2 and IGFBP3.
  • These findings reveal a coordinated cellular defense mechanism involving MxA and its cofactors against influenza A virus.

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