HIV-1 infection and induction of interferon alpha in plasmacytoid dendritic cellsBenlahrech, Adel; Patterson, StevenCurrent Opinion in HIV and AIDS: September 2011 - Volume 6 - Issue 5 - p 373–378 doi: 10.1097/COH.0b013e328349592a Innate immunity: Edited by William A. Paxton and Teunis B.H. Geijtenbeek Abstract Author Information 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. Department of Immunology, Imperial College London, Chelsea and Westminster Hospital, London, UK Correspondence to Steven Patterson, Immunology Section, Division of Infectious Diseases, Imperial College, Chelsea & Westminster Hospital, 369 Fulham Road, London, UKTel: +44 203 315 5934; fax: +44 203 315 5997; e-mail: email@example.com © 2011 Lippincott Williams & Wilkins, Inc.