title: HIV-1 infection and induction of interferon alpha in plasmacytoid dendritic cells.
abstract: OBJECTIVE
  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.
  
  
  RESULTS
  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.
  
  
  CONCLUSIONS
  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.
authors: Department of Immunology, Imperial College London, Chelsea and Westminster Hospital, London, UK.
authors: Adel
authors: A
authors: Benlahrech
authors: Steven
authors: S
authors: Patterson
mesh_terms: D003713:Dendritic Cells / Q000276:immunology*; D015658:HIV Infections / Q000276:immunology* / Q000821:virology*; D015497:HIV-1 / Q000276:immunology*; D006801:Humans; D016898:Interferon-alpha / Q000096:biosynthesis* / Q000276:immunology
chemical_list: D016898:Interferon-alpha