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About the Authors:
Erin H. Graf
Affiliation: Department of Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, United States of America
Matthew J. Pace
Affiliation: Department of Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, United States of America
Bennett A. Peterson
Affiliation: Laboratory of Immunoregulation, NIAID, National Institutes of Health, Bethesda, Maryland, United States of America
Lindsay J. Lynch
Affiliation: Department of Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, United States of America
Steve B. Chukwulebe
Affiliation: Department of Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, United States of America
Angela M. Mexas
Affiliation: Department of Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, United States of America
Farida Shaheen
Affiliation: Center for Aids Research, University of Pennsylvania, Philadelphia, Pennsylvania, United States of America
Jeffrey N. Martin
Affiliation: Department of Epidemiology and Biostatistics, University of California, San Francisco, San Francisco, California, United States of America
Steven G. Deeks
Affiliation: Department of Medicine, University of California, San Francisco, San Francisco, California, United States of America
Mark Connors
Affiliation: Laboratory of Immunoregulation, NIAID, National Institutes of Health, Bethesda, Maryland, United States of America
Stephen A. Migueles
Affiliation: Laboratory of Immunoregulation, NIAID, National Institutes of Health, Bethesda, Maryland, United States of America
Una O’Doherty
* E-mail: [email protected]
Affiliation: Department of Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, United States of America
Introduction
Resting CD4+ T cells harboring latent proviruses remain barriers to a cure for HIV [1–6]. As lifelong treatment with HAART is burdensome and cost prohibitive for many, strategies aimed at curing HIV are of great importance. While many strategies seek to clear reservoirs by stimulating HIV expression [7–11] recent data suggests that stimulation alone does not result in death of the infected cell [12]. Therefore, new approaches may be required to clear HIV reservoirs. Our group and others have turned to a unique population of HIV infected individuals who are able to control viremia without therapy [13–16] and appear to have smaller HIV reservoirs [17–19] (“elite controllers” or EC). Understanding how controllers maintain a low reservoir size may provide key insight into curing HIV [20].
We previously reported that CD4+ T cells from EC contain low levels of integrated HIV DNA (consistent with infrequent recovery of...