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Assembly and Purification of Prototype Foamy Virus Intasomes
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Alphavirus Restriction by IFITM Proteins.

Stuart Weston1, Stephanie Czieso1, Ian J White1

  • 1MRC Laboratory for Molecular Cell Biology, University College London, Gower Street, London, WC1E 6BT, UK.

Traffic (Copenhagen, Denmark)
|May 25, 2016
PubMed
Summary

Interferon inducible transmembrane proteins (IFITMs) restrict alphavirus infection by blocking viral fusion. IFITM3 is particularly effective, inhibiting viral entry at multiple cellular locations.

Keywords:
IFITMSFVSemliki Forest virusalphavirusinterferon inducible transmembrane proteinrestriction factorvirus entryvirus-host interaction

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Area of Science:

  • Virology
  • Cell Biology
  • Immunology

Background:

  • Interferon-inducible transmembrane proteins (IFITMs) are known broad-spectrum antiviral factors.
  • The precise mechanisms by which IFITMs inhibit viral entry remain incompletely understood and may differ across viral families.

Purpose of the Study:

  • To investigate the role of IFITM proteins in restricting alphavirus infection, specifically Sindbis virus (SINV) and Semliki Forest virus (SFV).
  • To elucidate the specific stage of viral entry inhibited by IFITMs, focusing on membrane fusion.

Main Methods:

  • Utilized cell culture models to assess the impact of IFITM1, IFITM2, and IFITM3 on SFV and SINV infection.
  • Investigated viral entry steps including binding, internalization, endosomal trafficking, and low pH-induced fusion.
  • Employed a mutant IFITM3 (Y20A) localized to the plasma membrane to study cell surface fusion events.

Main Results:

  • IFITM3 significantly restricted SFV and SINV infection mediated by endosomal acid-induced fusion.
  • IFITM3 inhibited the release of the SFV capsid into the cytoplasm without affecting earlier entry steps.
  • Both IFITM1 and IFITM3 inhibited SFV infection mediated by cell surface fusion, with IFITM3 showing greater potency.
  • IFITM3 demonstrated broader antiviral activity against SFV compared to IFITM1 and IFITM2.

Conclusions:

  • IFITM proteins, particularly IFITM3, restrict alphavirus infection by inhibiting viral fusion with host cell membranes.
  • IFITM3's antiviral efficacy is dependent on its cellular localization, with enhanced activity against cell surface fusion events.
  • These findings highlight IFITM3 as a potent intrinsic immunity factor against alphaviruses.