HIV-1 infection and induction of interferon alpha in plasmacytoid dendritic cells

Curr Opin HIV AIDS. 2011 Sep;6(5):373-8. doi: 10.1097/COH.0b013e328349592a.


Purpose of review: Loss of blood plasmacytoid dendritic cell (pDC) in HIV-1 infection is thought to impact on adaptive immune responses whilst the virus also induces aberrant interferon alpha (IFN-α) production that may fuel chronic immune activation and drive disease progression. Recent attention has focussed on the pathway of HIV-induced IFN-α production by pDC and the new data are reviewed here together with the pathway leading to infection.

Recent findings: Attachment to CD4 and chemokine co-receptors is essential for HIV-1 infection. Although CD4, but not co-receptor binding, is a major route for passage to endosomes and triggering of IFN-α secretion this may also occur by CD4-independent mechanisms involving other receptors. In contrast to other Toll-like receptor (TLR)-7 ligands and RNA viruses that stimulate pDC to secrete IFN-α for 2-3 h, HIV-1-stimulated pDC can give sustained IFN-α production for up to 48 h which may contribute to chronic immune activation. This may reflect retention of HIV in early endosomes which also seems to be associated with incomplete maturation induced by HIV.

Summary: HIV-1-pDC interactions contribute to pathogenesis through depletion and aberrant IFN-α production. New data on the pathway of pDC HIV-stimulated IFN-α secretion may facilitate therapy to reduce chronic immune activation and slow disease progression.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Dendritic Cells / immunology*
  • HIV Infections / immunology*
  • HIV Infections / virology*
  • HIV-1 / immunology*
  • Humans
  • Interferon-alpha / biosynthesis*
  • Interferon-alpha / immunology


  • Interferon-alpha