HIV-1 infection of human macrophages directly induces viperin which inhibits viral production

Blood. 2012 Jul 26;120(4):778-88. doi: 10.1182/blood-2012-01-407395. Epub 2012 Jun 7.

Abstract

Macrophages are key target cells for HIV-1. HIV-1(BaL) induced a subset of interferon-stimulated genes in monocyte-derived macrophages (MDMs), which differed from that in monocyte-derived dendritic cells and CD4 T cells, without inducing any interferons. Inhibition of type I interferon induction was mediated by HIV-1 inhibition of interferon-regulated factor (IRF3) nuclear translocation. In MDMs, viperin was the most up-regulated interferon-stimulated genes, and it significantly inhibited HIV-1 production. HIV-1 infection disrupted lipid rafts via viperin induction and redistributed viperin to CD81 compartments, the site of HIV-1 egress by budding in MDMs. Exogenous farnesol, which enhances membrane protein prenylation, reversed viperin-mediated inhibition of HIV-1 production. Mutagenesis analysis in transfected cell lines showed that the internal S-adenosyl methionine domains of viperin were essential for its antiviral activity. Thus viperin may contribute to persistent noncytopathic HIV-1 infection of macrophages and possibly to biologic differences with HIV-1-infected T cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Amino Acid Sequence
  • Antiviral Agents / metabolism
  • Biomarkers / metabolism
  • Blotting, Western
  • Dendritic Cells / cytology
  • Dendritic Cells / metabolism
  • Dendritic Cells / virology
  • Farnesol / pharmacology
  • Flow Cytometry
  • Gene Expression Profiling
  • HIV Infections / metabolism
  • HIV Infections / pathology
  • HIV Infections / virology*
  • HIV-1 / genetics
  • HIV-1 / pathogenicity*
  • Humans
  • Immunoenzyme Techniques
  • Immunoprecipitation
  • Interferons / metabolism
  • Macrophages / cytology
  • Macrophages / metabolism
  • Macrophages / virology*
  • Molecular Sequence Data
  • Monocytes / cytology
  • Monocytes / metabolism
  • Monocytes / virology*
  • Mutagenesis, Site-Directed
  • Mutation / genetics
  • Oligonucleotide Array Sequence Analysis
  • Oxidoreductases Acting on CH-CH Group Donors
  • Protein Prenylation
  • Proteins / antagonists & inhibitors
  • Proteins / genetics
  • Proteins / metabolism*
  • RNA, Messenger / genetics
  • RNA, Small Interfering / genetics
  • Real-Time Polymerase Chain Reaction
  • Reverse Transcriptase Polymerase Chain Reaction
  • Sequence Homology, Amino Acid
  • Virus Replication*

Substances

  • Antiviral Agents
  • Biomarkers
  • Proteins
  • RNA, Messenger
  • RNA, Small Interfering
  • Farnesol
  • Interferons
  • Oxidoreductases Acting on CH-CH Group Donors
  • RSAD2 protein, human