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CCL3L1 and HIV/AIDS susceptibility

Nature Medicine volume 15, pages 1110–1112 (2009)Cite this article

To the Editor:

We read with interest the recent article in Nature Medicine describing the influence of variation in CCL3L1 copy number and CCR5 genotype on immune recovery during highly active antiretroviral therapy (HAART) in HIV-1–infected individuals1. The chemotactic cytokine CCL3L1 (encoding the macrophage inflammatory protein-1αP (MIP-1αP) protein) is a potent ligand for the HIV-1 co-receptor CCR5, which is essential for viral entry into human host cells2. The recent study is part of a series that began in 2005 with a paper reporting effects of CCL3L1 copy number variation on HIV-1 acquisition, viral load and disease progression3, followed by several publications investigating clinically correlated phenotypes in a largely overlapping set of HIV-positive individuals1,4,5.

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Figure 1: CCL3L1 copy number estmiates and their relationship to HIV-1 viral load and CCL3L1 mRNA expression.

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Acknowledgements

Funding was provided by the US National Institutes of Health–funded CHAVI. J.F. is supported by the Swiss Foundation for Grants in Biology and Medicine, and A.T. is supported by Infectigen and the Swiss National Science Foundation. This project has been funded in whole or in part with federal funds from the US National Cancer Institute, National Institutes of Health, under contract N01-CO-12400. The content of this publication does not necessarily reflect the views or policies of the Department of Health and Human Services, nor does mention of trade names, commercial products or organizations imply endorsement by the US government. This research was supported in part by the Intramural Research Program of the National Institutes of Health, National Cancer Institute, Center for Cancer Research.

Author information

Authors and Affiliations

  1. Center for Human Genome Variation, Duke Institute for Genome Sciences and Policy, Duke University, Durham, North Carolina, USA

    Thomas J Urban, Jacques Fellay, Curtis Gumbs, Kimberly Pelak, Kristen K Dang & David B Goldstein

  2. Infectious Disease Clinical Research Program, Walter Reed Army Medical Center, Washington, DC, USA

    Amy C Weintrob

  3. Institute of Microbiology, University Hospital Center, and University of Lausanne, Lausanne, Switzerland

    Sara Colombo, Margalida Rotger & Amalio Telenti

  4. Duke Institute for Genome Sciences and Policy, Duke University, Durham, North Carolina, USA

    Kevin V Shianna

  5. Department of Medicine, David Geffen School of Medicine, University of California at Los Angeles, Los Angeles, California, USA

    Roger Detels

  6. Department of Infectious Diseases and Microbiology, University of Pittsburgh, Pittsburgh, Pennsylvania, USA

    Jeremy J Martinson

  7. Laboratory of Genomic Diversity, National Cancer Institute at Frederick, Frederick, Maryland, USA

    Stephen J O'Brien

  8. Division of Viral Pathogenesis, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA

    Norman L Letvin

  9. Medical Research Council Human Immunology Unit, Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, Oxford, UK

    Andrew J McMichael

  10. Duke Human Vaccine Institute, Duke University, Durham, North Carolina, USA

    Barton F Haynes

  11. Cancer and Inflammation Program, Laboratory of Experimental Immunology, SAIC-Frederick, Inc., National Cancer Institute at Frederick, Frederick, Maryland, USA

    Mary Carrington

  12. Division of Retrovirology, Walter Reed Army Institute of Research, US Military HIV Research Program, Rockville, Maryland, USA

    Nelson L Michael

  13. Center for HIV/AIDS Vaccine Immunology (CHAVI) and the Euro-CHAVI consortia,

    Amalio Telenti & David B Goldstein

  14. Multicenter AIDS Cohort Study (MACS),

    Roger Detels & Jeremy J Martinson

  15. Tri-Service AIDS Clinical Consortium (TACC) of the Infectious Disease Clinical Research Program,

    Amy C Weintrob & Nelson L Michael

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  1. Thomas J Urban
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Corresponding author

Correspondence to David B Goldstein.

Supplementary information

Supplementary Figures, Tables and Methods

Supplementary Figures 1–5, Supplementary Tables 1–4 and Supplementary Methods (PDF 392 kb)

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Urban, T., Weintrob, A., Fellay, J. et al. CCL3L1 and HIV/AIDS susceptibility. Nat Med 15, 1110–1112 (2009). https://doi.org/10.1038/nm1009-1110

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