IMMUNE ACTIVATION: Edited by Irini Sereti and Marcus AltfeldRole of immune activation in progression to AIDSUtay, Netanya S.; Hunt, Peter W.Author Information aUniversity of Texas Medical Branch, Galveston, Texas bUniversity of California San Francisco, California, USA Correspondence to Netanya S. Utay, MD, University of Texas Medical Branch, 301 University Blvd Rte 0435, Galveston, TX 77555, USA. Tel: +1 409 747 0240; fax: +1 409 772 6527; e-mail: firstname.lastname@example.org Current Opinion in HIV and AIDS: March 2016 - Volume 11 - Issue 2 - p 131-137 doi: 10.1097/COH.0000000000000242 Buy Metrics Abstract Purpose of review The purpose is to review recent insights into the impact of HIV-associated immune activation on AIDS and non-AIDS morbidity and mortality. Recent findings Immune activation has long been recognized as an important consequence of untreated HIV infection and predictor of AIDS progression, which declines but fails to normalize during suppressive antiretroviral therapy, and continues to predict disease in this setting. Thus, a major research agenda is to develop novel therapies to reduce persistent immune activation in treated HIV infection. Yet, the optimal targets for interventions remain unclear. Both the specific root causes of immune activation and the many interconnected pathways of immune activation that are most likely to drive disease risk in HIV-infected individuals remain incompletely characterized, but recent studies have shed new light on these topics. Summary In the context of this review, we will summarize recent evidence helping to elucidate the immunologic pathways that appear most strongly predictive of infectious and noninfectious morbidity. We will also highlight the likelihood that not all root drivers of immune activation – and the discrete immunologic pathways to which they give rise – are likely to produce the same disease manifestations and/or be equally attenuated by early antiretroviral therapy initiation. Copyright © 2016 Wolters Kluwer Health, Inc. All rights reserved.