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CCL3L1 and HIV/AIDS susceptibility

Nature Medicine volume 15, pages 1112–1115 (2009)Cite this article

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To the Editor:

A selective advantage against infectious diseases such as HIV/AIDS is associated with differences in the genes relevant to immunity and virus replication. The CC chemokine receptor-5 (CCR5), the principal co-receptor for HIV, and its chemokine ligands, including CC chemokine ligand-3–like-1 (CCL3L1), influence the susceptibility of the CD4+ target cell to infection1. The CCL3L1 gene is one of several cytokine genes clustered in a region of segmental duplication on chromosome 17q12 (ref. 2). The CCL3L1 gene copy number per diploid genome varies between people and among persons of various geographical ancestries2,3,4,5; some people have a partial CCL3L1 pseudogene as well2. Evidence has been presented that increased CCL3L1 gene copy numbers can have marked phenotypic consequences for HIV/AIDS pathogenesis as a result of altering gene dosage3,4,5. We have been unable to reproduce these findings using the same methods in a different cohort.

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Figure 1: HIV disease–influencing effect associated with number of CCL3L1 gene copies during the pre-HAART era.

Change history

  • 03 November 2009

    In the version of this supplementary file originally posted online, the DNA sequence of the probe for real-time PCR quantification of CCL3L1 gene copy number was incorrect. The error has been corrected in this file as of 3 November 2009.

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Acknowledgements

We thank B. Korber for assistance with the figures. This work is funded by the US National Institutes of Health (AI-35039 to S.M.W. and J.P.P.).

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Authors and Affiliations

  1. Santa Fe Institute, Santa Fe, New Mexico, USA

    Tanmoy Bhattacharya

  2. Los Alamos National Laboratory, Los Alamos, New Mexico, USA

    Tanmoy Bhattacharya

  3. Division of Infectious Diseases, The Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA

    Jennifer Stanton, Eun-Young Kim, Kevin J Kunstman, John P Phair & Steven M Wolinsky

  4. Department of Epidemiology, Johns Hopkins University Bloomberg School of Public Health, Baltimore, Maryland, USA

    Lisa P Jacobson

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  1. Tanmoy Bhattacharya
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  2. Jennifer Stanton
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Correspondence to Steven M Wolinsky.

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Supplementary Figures 1–2 and Supplementary Methods (PDF 803 kb)

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Bhattacharya, T., Stanton, J., Kim, EY. et al. CCL3L1 and HIV/AIDS susceptibility. Nat Med 15, 1112–1115 (2009). https://doi.org/10.1038/nm1009-1112

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