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Amphotericin B increases influenza A virus infection by preventing IFITM3-mediated restriction

Tsai-Yu Lin1, Christopher R Chin2, Aaron R Everitt3

  • 1Department of Microbiology and Physiological Systems, University of Massachusetts Medical School, Worcester, MA 01655, USA.

Cell Reports
|November 26, 2013
PubMed

Insights

Amphotericin B (AmphoB), an antifungal drug, unexpectedly enhances influenza A virus (IAV) replication by blocking IFITM3's antiviral activity. This finding suggests patients on AmphoB therapy may be more vulnerable to IAV infections.

Area of Science:

  • Virology
  • Immunology
  • Pharmacology

Background:

  • Interferon-induced transmembrane proteins (IFITMs) are crucial for innate immunity against influenza A virus (IAV).
  • IFITM3 specifically restricts IAV replication, contributing to host defense.
  • The precise mechanisms by which IFITMs exert their antiviral effects are still being elucidated.

Purpose of the Study:

  • To investigate the effect of the antifungal drug amphotericin B (AmphoB) on IFITM-mediated restriction of IAV.
  • To determine if clinical preparations of AmphoB impact host defense against IAV.
  • To elucidate the mechanism by which AmphoB interferes with IFITM antiviral activity.

Main Methods:

  • In vitro assays measuring IAV replication in the presence of IFITM proteins and AmphoB.
  • In vivo studies using a mouse model of IAV infection treated with AmBisome (a clinical AmphoB preparation).
  • Analysis of host membrane fluidity in response to IFITM1 expression and AmphoB treatment.

Main Results:

  • AmphoB and its clinical formulation AmBisome prevent IFITM3-mediated restriction of IAV, leading to increased viral replication.
  • AmphoB neutralizes the protective effect of interferon against IAV in vitro.
  • IFITM1 was found to decrease host membrane fluidity, a property negated by AmphoB.
  • Mice treated with AmBisome exhibited increased susceptibility to IAV infection, mirroring outcomes in Ifitm3-deficient mice.

Conclusions:

  • AmphoB interferes with the antiviral functions of IFITM proteins, particularly IFITM3.
  • Clinical use of AmphoB may compromise host defense against IAV and potentially other IFITM3-restricted viruses.
  • Patients undergoing antifungal therapy with AmphoB may be functionally immunocompromised, increasing their vulnerability to viral infections.

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