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Mx proteins: antiviral gatekeepers that restrain the uninvited

Judith Verhelst1, Paco Hulpiau, Xavier Saelens

  • 1Address correspondence to Xavier Saelens, xavier.saelens@dmbr.vib-ugent.be.

Microbiology and Molecular Biology Reviews : MMBR
|December 4, 2013
PubMed

Insights

Mx proteins, crucial for antiviral defense, are large GTPases that inhibit diverse viruses by forming ring structures. This mechanism likely involves binding viral ribonucleoprotein complexes, disrupting their function.

Area of Science:

  • Virology
  • Molecular Biology
  • Immunology

Background:

  • Mx proteins are conserved dynamin-like GTPases essential for innate antiviral immunity.
  • Their expression is interferon-inducible, and they target a broad range of viruses, particularly negative-stranded RNA viruses.
  • The precise molecular mechanisms underlying their broad antiviral activity remain incompletely understood.

Purpose of the Study:

  • To elucidate the molecular mechanisms by which Mx proteins exert their broad-spectrum antiviral activity.
  • To investigate the role of GTPase activity and protein oligomerization in Mx antiviral function.
  • To propose a model for Mx protein interaction with viral targets.

Main Methods:

  • Phylogenetic analysis of Mx genes across vertebrates.
  • Structural analyses of Mx proteins.
  • Biochemical assays to study GTPase activity and oligomerization.
  • Hypothetical modeling of Mx-viral complex interactions.

Main Results:

  • Mx proteins are present in most vertebrates, encoded by one to three gene copies.
  • GTPase activity is indispensable for the antiviral function of Mx proteins.
  • Structural insights suggest Mx proteins may interact with viral ribonucleoprotein complexes.
  • A model proposes Mx ring formation around viral complexes, leading to disassembly.

Conclusions:

  • Mx proteins function as antiviral effectors through a conserved mechanism involving GTPase-dependent oligomerization.
  • The proposed model of Mx ring assembly around viral ribonucleoprotein complexes explains their broad target specificity.
  • These findings advance our understanding of innate antiviral immunity and potential therapeutic strategies.

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