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Current Opinion in HIV & AIDS:
doi: 10.1097/COH.0b013e328349592a
Innate immunity: Edited by William A. Paxton and Teunis B.H. Geijtenbeek

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

Benlahrech, Adel; Patterson, Steven

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Abstract

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.

© 2011 Lippincott Williams & Wilkins, Inc.

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