Papers in the Biological Sciences



Mohamed Abdel-Mohsen, The Wistar Institute
Leticia Kuri-Cervantes, University of Pennsylvania
Judith Grau-Exposito, Universitat Autònoma de Barcelona
Adam M. Spivak, University of Utah School of Medicine
Racheal A. Nell, University of Utah School of Medicine
Costin Tomescu, The Wistar Institute
Surya Kumari Vadrevu, The Wistar Institute
Leila B. Giron, The Wistar Institute
Carla Serra-Peinado, Universitat Autònoma de Barcelona
Meritxell Genesca, Universitat Autònoma de Barcelona
Josep Castellvi, Hospital Universitari Vall d´Hebrón
Guoxin Wu, Merck & Co. Inc.
Perla M. Del Rio Estrada, Instituto Nacional de Enfermedades Respiratorias
Mauricio Gonzalez-Navarro, Instituto Nacional de Enfermedades Respiratorias
Kenneth Lynn, The Wistar Institute
Collin T. King, Emory University
Sai Vemula, Merck & Co. Inc.
Kara Cox, Merck & Co. Inc.
Yanmin Wan, University of Nebraska - Lincoln
Qingsheng Li, University of Nebraska-LincolnFollow
Karam Mounzer, Jonathan Lax Center, Philadelphia FIGHT
Jay Kostman, Jonathan Lax Center, Philadelphia FIGHT
Ian Frank, University of Pennsylvania
Mirko Paiardini, Emory University
Daria Hazuda, Merck & Co. Inc.
Gustavo Reyes-Teran, Instituto Nacional de Enfermedades Respiratorias
Douglas Richman, Veterans Affairs San Diego Healthcare System and University of California
Bonnie Howell, Merck & Co. Inc.
Pablo Tebas, University of Pennsylvania
Javier Martinez-Picado, IrsiCaixa AIDS Research Institute
Vicente Planelles, University of Utah School of Medicine
Maria J. Buzon, Universitat Autònoma de BarcelonaFollow
Michael R. Betts, University of PennsylvaniaFollow
Luis J. Montaner, The Wistar InstituteFollow

Date of this Version



Sci. Transl. Med. 10, eaar6759 (2018)


Copyright © 2018 The Authors

This document is a U.S. government work and is not subject to copyright in the United States.

DOI: 10.1126/scitranslmed.aar6759


The persistence of HIV reservoirs, including latently infected, resting CD4+ T cells, is the major obstacle to cure HIV infection. CD32a expression was recently reported to mark CD4+ T cells harboring a replication-competent HIV reservoir during antiretroviral therapy (ART) suppression. We aimed to determine whether CD32 expression marks HIV latently or transcriptionally active infected CD4+ T cells. Using peripheral blood and lymphoid tissue of ART-treated HIV+ or SIV+ subjects, we found that most of the circulating memory CD32+ CD4+ T cells expressed markers of activation, including CD69, HLA-DR, CD25, CD38, and Ki67, and bore a TH2 phenotype as defined by CXCR3, CCR4, and CCR6. CD32 expression did not selectively enrich for HIV- or SIV-infected CD4+ T cells in peripheral blood or lymphoid tissue; isolated CD32+ resting CD4+ T cells accounted for less than 3% of the total HIV DNA in CD4+ T cells. Cell-associated HIV DNA and RNA loads in CD4+ T cells positively correlated with the frequency of CD32+ CD69+ CD4+ T cells but not with CD32 expression on resting CD4+ T cells. Using RNA fluorescence in situ hybridization, CD32 coexpression with HIV RNA or p24 was detected after in vitro HIV infection (peripheral blood mononuclear cell and tissue) and in vivo within lymph node tissue from HIV-infected individuals. Together, these results indicate that CD32 is not a marker of resting CD4+ T cells or of enriched HIV DNA–positive cells after ART; rather, CD32 is predominately expressed on a subset of activated CD4+ T cells enriched for transcriptionally active HIV after long-term ART.

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