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The Engagement of Activating FcRs Inhibits Primate Lentivirus Replication in Human Macrophages¹

Annie David^*, Asier Sáez-Cirión^*, Pierre Versmisse^*, Odile Malbec^,, Bruno Iannascoli^,, Florence Herschke^*, Marianne Lucas, Françoise Barré-Sinoussi^*, Jean-François Mouscadet^¶, Marc Daëron^, and Gianfranco Pancino^2,*

^* Unité de Régulations des Infections Rétrovirales, Institut Pasteur, Paris, France; Unité d’Allergologie Moléculaire et Cellulaire, Institut Pasteur, Paris, France; Institut National de la Santé et de la Recherche Médicale Unité 760, Paris, France; Unité Postulante Interactions Moléculaires Flavivirus-Hôtes, Institut Pasteur, Paris, France; and ^¶ Laboratoire de Biotechnologies et de Pharmacologie génétique Appliquée-Centre National de la Recherche Scientifique, Unité Mixte de Recherche 8113, Ecole Normale Supérieure de Cachan, Cachan, France

We previously reported that the stimulation of monocyte-derived macrophages (MDM) by plate-bound i.v. Igs inhibits HIV-1 replication. In this study, we show that IgG immune complexes also suppress HIV-1 replication in MDMs and that activating receptors for the Fc portion of IgG–FcRI, FcRIIA, and FcRIII–are responsible for the inhibition. MDM stimulation through FcRs induces activation signals and the secretion of HIV-1 modulatory cytokines, such as M-CSF, TNF-, and macrophage-derived chemokine. However, none of these cytokines contribute to HIV-1 suppression. HIV-1 entry and postintegration steps of viral replication are not affected, whereas reduced levels of reverse transcription products and of integrated proviruses, as determined by real-time PCR analysis, account for the suppression of HIV-1 gene expression in FcR-activated MDMs. We found that FcR-dependent activation of MDMs also inhibits the replication of HIV-2, SIVmac, and SIVagm, suggesting a common control mechanism for primate immunodeficiency lentiviruses in activated macrophages.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported by the Agence Nationale de Recherches sur le SIDA, France.

² Address correspondence and reprint requests to Dr. Gianfranco Pancino, Unité de Régulations des Infections Rétrovirales, Institut Pasteur, 25, rue du Docteur Roux, 75726 Paris Cedex 15, France. E-mail address: gpancino{at}pasteur.fr

³ Abbreviations used in this paper: IVIg, i.v. Ig; IC, immune complex; rtPCR, real-time PCR; MDM, monocyte-derived macrophage; RBL, rat basophilic leukemia; MDC, macrophage-derived chemokine; PLC, phospholipase C; m.o.i., multiplicity of infection; WN, West Nile; RT, reverse transcription; p.i., postinfection.

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