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The role of CD32 during HIV-1 infection

Nature volume 561, pages E17–E19 (2018)Cite this article

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arising from B. Descours et al. Nature 543, 564–567 (2017); https://doi.org/10.1038/nature21710

The persistence of latent HIV-1 in resting memory CD4+ T cells is a major barrier to a cure, and a biomarker for latently infected cells would be of great scientific and clinical importance1,2,3,4,5. Using an elegant discovery-based approach, Descours et al.6 reported that CD32a, an Fcγ receptor not normally expressed on T cells, is a potential biomarker for the HIV-1 reservoir in CD4+ T cells6. Using a quantitative viral outgrowth assay (qVOA), we show that CD32+CD4+ T cells do not contain the majority of intact proviruses in the latent reservoir and that the enrichment found by Descours et al.6 may in part reflect the use of an ultrasensitive ELISA that does not predict exponential viral outgrowth. Our studies show that CD32 is not a biomarker for the major population of latently infected CD4+ T cells. There is a Reply to this Comment by Descours, B. et al. Nature 561, https://doi.org/10.1038/s41586-018-0496-1 (2018).

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Fig. 1: Analysis of CD4+CD32- and CD4+CD32+ populations by qVOA and proviral DNA measurements.
Fig. 2: Ultrasensitive p24 measurements.

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Authors and Affiliations

  1. Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA

    Lynn N. Bertagnolli, Jennifer A. White, Francesco R. Simonetti, Subul A. Beg, Jun Lai, Alexandra J. Murray, Annukka A. R. Antar, Robert F. Siliciano, Gregory M. Laird & Janet D. Siliciano

  2. Howard Hughes Medical Institute, Baltimore, MD, USA

    Subul A. Beg, Jun Lai & Robert F. Siliciano

  3. The Wistar Institute, Philadelphia, PA, USA

    Costin Tomescu & Luis J. Montaner

  4. Department of Molecular Microbiology and Immunology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA

    Hao Zhang & Joseph B. Margolick

  5. Division of HIV, Infectious Diseases and Global Medicine, University of California, San Francisco, CA, USA

    Rebecca Hoh & Stephen G. Deeks

  6. Division of Infectious Diseases, Department of Medicine, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA, USA

    Pablo Tebas

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  1. Lynn N. Bertagnolli
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Contributions

L.N.B., J.A.W., G.M.L., F.R.S., R.F.S. and J.D.S. designed experiments. S.A.B., C.T. and L.J.M. obtained samples. L.N.B., J.A.W., S.A.B., G.M.L., F.R.S., J.L., A.J.M., A.A.R.A. and J.D.S. performed experiments. F.R.S., H.J. and J.B.M. performed cell sorting. L.N.B., J.A.W., F.R.S., A.J.M., A.A.R.A., R.F.S. and J.D.S. analysed the data and wrote the manuscript.

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Correspondence to Robert F. Siliciano.

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This file contains Supplementary Tables 1-3, Supplementary Figures 1-2 and the Supplementary Methods.

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Bertagnolli, L.N., White, J.A., Simonetti, F.R. et al. The role of CD32 during HIV-1 infection. Nature 561, E17–E19 (2018). https://doi.org/10.1038/s41586-018-0494-3

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