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 Blood, 28 May 2009, Vol. 113, No. 22, pp. 5497-5505.
Prepublished online as a Blood First Edition Paper on March 19, 2009; DOI 10.1182/blood-2008-11-190231.

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IMMUNOBIOLOGY

Desensitization to type I interferon in HIV-1 infection correlates with markers of immune activation and disease progression

Gareth A. D. Hardy1, Scott F. Sieg2,3, Benigno Rodriguez2,3, Wei Jiang2, Robert Asaad2,3, Michael M. Lederman13, and Clifford V. Harding1,3

1 Department of Pathology, 2 Division of Infectious Disease, and 3 Center for AIDS Research, Case Western Reserve University and University Hospitals Case Medical Center, Cleveland, OH

Type I interferon (IFN{alpha}/β) plays a complex role in HIV-1 infection and has been proposed alternately to have roles in either disease protection or progression. Although IFN{alpha}/β plays crucial roles in regulating monocytes and dendritic cells, responsiveness of these cells to IFN{alpha}/β in HIV-1 infection is poorly understood. We report significant defects in IFN{alpha}/β receptor (IFN{alpha}/βR) expression, IFN{alpha} signaling, and IFN{alpha}-induced gene expression in monocytes from HIV-1–infected subjects. IFN{alpha}/βR expression correlated directly with CD4+ T-cell count and inversely with HIV-1 RNA level and expression of CD38 by memory (CD45RO+) CD8+ T cells, a measure of pathologic immune activation in HIV-1 infection associated with disease progression. In addition, monocytes from HIV-1–infected persons showed diminished responses to IFN{alpha}, including decreased induction of phosphorylated STAT1 and the classical interferon-stimulated gene produces MxA and OAS. These IFN{alpha} responses were decreased regardless of IFN{alpha}/βR expression, suggesting that regulation of intracellular signaling may contribute to unresponsiveness to IFN{alpha}/β in HIV-1 disease. Defective monocyte responses to IFN{alpha}/β may play an important role in the pathogenesis of HIV-1 infection, and decreased IFN{alpha}/βR expression may serve as a novel marker of disease progression.


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