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Correspondence
Nature Medicine 15, 1112 - 1115 (2009)
doi:10.1038/nm1009-1112
CCL3L1 and HIV/AIDS susceptibility
Tanmoy Bhattacharya1,2, Jennifer Stanton3, Eun-Young Kim3, Kevin J Kunstman3, John P Phair3, Lisa P Jacobson4 & Steven M Wolinsky3
- Santa Fe Institute, Santa Fe, New Mexico, USA.
- Los Alamos National Laboratory, Los Alamos, New Mexico, USA.
- Division of Infectious Diseases, The Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA.
- Department of Epidemiology, Johns Hopkins University Bloomberg School of Public Health, Baltimore, Maryland, USA.
Correspondence to: Steven M Wolinsky3 e-mail: s-wolinsky@northwestern.edu
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.
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