A cryptic sensor for HIV-1 activates antiviral innate immunity in dendritic cells

Nicolas Manel, Brandon Hogstad, Yaming Wang, David E. Levy, Derya Unutmaz and Dan R. Littman ()
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Nicolas Manel: Molecular Pathogenesis Program, The Kimmel Center for Biology and Medicine of the Skirball Institute, New York University School of Medicine
Brandon Hogstad: Molecular Pathogenesis Program, The Kimmel Center for Biology and Medicine of the Skirball Institute, New York University School of Medicine
Yaming Wang: New York University School of Medicine
David E. Levy: New York University School of Medicine
Derya Unutmaz: New York University School of Medicine
Dan R. Littman: Molecular Pathogenesis Program, The Kimmel Center for Biology and Medicine of the Skirball Institute, New York University School of Medicine

Nature, 2010, vol. 467, issue 7312, 214-217

Abstract: HIV-1 in dendritic cells HIV-1 (human immunodeficiency virus 1) infection fails to induce interferon in the cells that it infects, but the underlying mechanisms involved are undefined. Dendritic cells — immune cells found in skin, mucosa and lymph tissues — mediate the innate detection of pathogens and the activation of other immune cells involved in specific adaptive immunity. But not for HIV. Dendritic cells are resistant to infection by HIV, although they do bind to the virus and are thought to facilitate the infection of T-helper cells. Now it is shown that when the usual block to HIV infection is bypassed in dendritic cells — by exposure to the Vpx accessory protein from the simian immunodeficiency virus SIVmac — HIV does induce a type I interferon response and T-cell activation. The virulence of HIV-1 may be related to its ability to evade innate immunity by staying out of dendritic cells, and the manipulation of that strategy may be of relevance to vaccine design.

Date: 2010
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DOI: 10.1038/nature09337

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