IMMUNE ACTIVATION: Edited by Irini Sereti and Marcus AltfeldResidual inflammation and viral reservoirs alliance against an HIV cureMassanella, Marta; Fromentin, Rémi; Chomont, NicolasAuthor Information aDepartment of Microbiology, Infectiology and Immunology, Faculté de Médecine, Université de Montréal bCentre de Recherche du CHUM, Montréal, Quebec, Canada *Marta Massanella and Rémi Fromentin equally contributed to the writing of this article. Correspondence to Nicolas Chomont, Centre de Recherche du CHUM, Université de Montréal, 900 rue St-Denis, QC H2X0A9, Canada. Tel: +1 514 890 8000 x31266; e-mail: [email protected] Current Opinion in HIV and AIDS: March 2016 - Volume 11 - Issue 2 - p 234-241 doi: 10.1097/COH.0000000000000230 Buy Metrics Abstract Purpose of review HIV persists in cellular and anatomical reservoirs during antiretroviral therapy (ART). Viral persistence is ensured by a variety of mechanisms including ongoing viral replication and proliferation of latently infected cells. In this review, we summarize recent findings establishing a link between the unresolved levels of inflammation observed in virally suppressed individuals on ART and the mechanisms responsible for HIV persistence. Recent findings Residual levels of viral replication during ART are associated with persistent low levels of immune activation, suggesting that unresolved inflammation can promote the replenishment of the HIV reservoir in tissues. In addition, the recent findings that the latent HIV reservoir is maintained by continuous proliferation of latently infected cells provide another mechanism by which residual inflammation could contribute to HIV persistence. Summary Residual inflammation during ART is likely to be a critical parameter contributing to HIV persistence. Therefore, reducing inflammation may be an efficient way to interfere with the maintenance of the HIV reservoir in virally suppressed individuals on ART. Copyright © 2016 Wolters Kluwer Health, Inc. All rights reserved.