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 Blood, 5 February 2009, Vol. 113, No. 6, pp. 1278-1286.
Prepublished online as a Blood First Edition Paper on October 7, 2008; DOI 10.1182/blood-2008-06-161869.

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IMMUNOBIOLOGY

Cell adhesion through {alpha}V-containing integrins is required for efficient HIV-1 infection in macrophages

Ester Ballana1,*, Eduardo Pauls1,*, Jordi Senserrich1, Bonaventura Clotet1, Françoise Perron-Sierra2, Gordon C. Tucker2, and José A. Esté1

1 Retrovirology Laboratory IrsiCaixa, Hospital Universitari Germans Trias i Pujol, Universitat Autònoma de Barcelona, Badalona, Spain; and 2 Departments of Medicinal Chemistry and Cancer Research and Drug Discovery, Institut de Recherches Servier, Croissy sur Seine, France

Monocytes and macrophages are an important reservoir of human immunodeficiency virus (HIV) and may represent the largest reservoir of this virus in tissues. Differentiation of monocytes into macrophages leads to cell attachment and susceptibility to infection and replication of HIV. Among other cell-surface molecules, integrins are overexpressed during monocyte-macrophage differentiation and may play a role in the replication cycle of envelope viruses including HIV. Here, we show that inhibition of {alpha}V integrin in monocyte-derived macrophages, by RNA interference or their inhibition by a selective small heterocyclic RGD-mimetic nonpeptide compound, inhibited the replication of HIV in the absence of cytotoxicity. Interference or inhibition of {alpha}V integrins triggered a signal transduction pathway, leading to down-regulation of nuclear factor-{kappa}B–dependent HIV-1 transcription. Such inhibition was mediated by a MAP-kinase signaling cascade, probably involving ERK1/2, p38-mitogen–activated protein kinases, and HSP27. In conclusion, our results reveal a significant role of integrin {alpha}V-mediated adhesion in HIV-1 infection of macrophages.


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Related Article in Blood Online:

Integrating integrins into HIV pathogenesis
Andrea Lisco and Leonid Margolis
Blood 2009 113: 1207-1208. [Full Text] [PDF]





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