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Antiviral activity of bone morphogenetic proteins and activins

Lucy A Eddowes1, Kinda Al-Hourani1, Narayan Ramamurthy2

  • 1MRC Human Immunology Unit, MRC Weatherall Institute of Molecular Medicine, University of Oxford, John Radcliffe Hospital, Oxford, UK.

Nature Microbiology
|December 5, 2018
PubMed

Insights

Bone morphogenetic proteins (BMPs) and activins play a crucial role in controlling viral infections like hepatitis C virus (HCV). These proteins enhance cellular antiviral immunity, working both independently and in concert with interferon signaling.

Area of Science:

  • Virology
  • Immunology
  • Cell Biology

Background:

  • Chronic hepatitis C virus (HCV) infection is linked to reduced hepcidin expression, a process regulated by bone morphogenetic protein (BMP)/SMAD signaling.
  • The interaction between HCV infection and the BMP/SMAD pathway is antagonistic, impacting iron metabolism and immune response.

Purpose of the Study:

  • To investigate the role of the BMP/SMAD pathway in cellular antiviral immunity against viral infections.
  • To determine how BMPs and activins influence the response to interferon (IFN) and viral replication.

Main Methods:

  • Analysis of hepcidin expression in HCV-infected patients and cell culture models.
  • Investigating the effect of BMP6 on gene expression, including interferon regulatory factors (IRFs) and USP18.
  • Chromatin immunoprecipitation to identify SMAD1 binding sites.
  • Assessing the functional impact of BMP6 and activins on viral replication (HCV, HBV, Zika virus) alone and in combination with IFN.

Main Results:

  • HCV infection blunts BMP6-induced hepcidin expression, partly via TNF-mediated downregulation of the BMP co-receptor haemojuvelin.
  • Disruption of the BMP6/hepcidin axis and BMP/SMAD pathway variations in HCV patients correlate with infection outcomes.
  • BMP6 modulates a gene expression profile similar to type I interferon signaling, upregulating IRFs and downregulating USP18.
  • BMP6 enhances the transcriptional and antiviral response to IFN and directly inhibits HCV replication independently of IFN.
  • BMP6 and activin A inhibit HBV replication, and activin A inhibits Zika virus replication.

Conclusions:

  • The BMP/SMAD pathway is a critical regulator of cellular antiviral immunity, influencing both innate and adaptive immune responses.
  • BMPs and activins possess potent antiviral activities that are independent of and can modulate interferon signaling.
  • These findings reveal a significant, previously unappreciated role for BMPs and activins in combating viral infections.

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