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Author Notes:

Corresponding author. montaner@wistar.org (L.J.M.); mariajose.buzon@vhir.org (M.J.B.); betts@pennmedicine.upenn.edu (M.R.B.).

M.A.-M., L.K.-C., J.G.-E., A.M.S., R.A.N., C.T., S.K.V., L.B.G., C.S.-P., M.G., J.C., G.W., K.C., M.P., D.H., G.R.-T., B.H., P.T., J.M.-P., V.P., M.R.B., M J.B., C.T.K., and LJ.M. designed and carried out experiments.

M.A.-M., L.K.-C., J.G.-E., A.M.S., C.T., S.K.V., C.S.-P., M.G., S.V., K.C., M.P., Q.L., Y.W., D.H., G.R.-T., D.R., B.H., P.T., J.M.-P., V.P., M J.B., M.R.B., and LJ.M. analyzed and interpreted data.

P.M.D.R.E., M.G.-N., K.L., K.M., J.K., I.F., G.R.-T., J.C., and P.T. selected study subjects and provided samples.

M.A.-M., L.K.-C., A.M.S., J.M.-P., V.P., M J.B., M.R.B., and L.J.M. drafted the manuscript.

L.J.M. supervised/supported experimental data collection, coordinated integration of collaboration between all participating laboratories, and contributed and coordinated the drafting of the manuscript.

All authors edited the final version of the manuscript.

We thank the HIV-1 patients who participated in the study and their providers; Y. A. Luna, M. F. Torres, S. P. Astorga Melendez, M. Becerril, V. Falcó, R. Willekens, and J. Navarro for referral of patients and sample collection; M. Buggert for critical evaluation of flow cytometric data; J. G. Prado for providing the viral stock R5-Bal; L. Luque and M. Fernández for technical assistance; and M. Ostrowski at the University of Toronto for providing HIV-infected PBMC samples.

Competing interests: D.H. is a Merck employee and stockholder; I.F. served on the advisory board for Gilead Sciences and ViiV Healthcare; D.R. has consulted for Gilead, Antiva, and Monogram; and J.K. is a consultant at Gilead Sciences. All other authors declare that they have no competing interests.


Research Funding:

This work was supported by NIH R01 AI065279,U01 AI065279, and UM1 AI126620 (to LJ.M.); NIH R21 AI129636 and R21 NS106970 (to M.A.-M.); W. W. Smith Charitable Trust grant no. A17101 (to M.A.-M.); the Penn Center for AIDS Research (CFAR) (P30 AI 045008 to M.A.-M.); R21AI118411 (to M J.B.); NIH R01 AI124843 (to V.P.); the Spanish Secretariat of Science and Innovation and FEDER funds (grants SAF2015–67334-R to M.J.B. and SAF2016–80033-R to J.M.-P.); and GeSIDA and the Spanish AIDS network Red Temática Cooperativa de nvestigación en SIDA (RD16/0025/0007 to M J.B. and J.M.-P.).

Additional support was provided by the Miguel Servet program funded by the Spanish Health Institute Carlos III (CP17/00179), the Spanish “Ministerio de Economía y Competitividad, Instituto de Salud Carlos III” (ISCIII, PI17/01470), the “Pla estratègic de recerca i innovació en salut” (PERIS), from the Catalan government for M.G., Collaboratory of AIDS Researchers for Eradication (CARE; UM1AI126619), BEAT-HIV (1UM1Al126620), the University of California, San Diego CFAR (AI306214), the Department of Veterans Affairs, and the James B. Pendleton Charitable Trust.

Additional support was provided by The Philadelphia Foundation(Robert I. Jacobs Fund), Kean Family Professorship, Henry S. Miller Jr. and J. Kenneth Nimblett, AIDS funds from the Commonwealth of Pennsylvania and the Commonwealth Universal Research Enhancement Program, Pennsylvania Department of Health, the Penn CFAR (P30 AI 045008), and Cancer Center Grant (P30 CA10815).


  • Science & Technology
  • Life Sciences & Biomedicine
  • Cell Biology
  • Medicine, Research & Experimental
  • Research & Experimental Medicine

CD32 is expressed on cells with transcriptionally active HIV but does not enrich for HIV DNA in resting T cells

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Journal Title:

Science Translational Medicine


Volume 10, Number 437


Type of Work:

Article | Post-print: After Peer Review


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 m ark 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 H IV 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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© 2018 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science.

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