Reply to: Experimental aspects of copy number variant assays at CCL3L1

Abstract

We read with interest the recent article in Nature Medicine describingthe influence of variation in CCL3L1 copy number and CCR5 genotypeon 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, whichis 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 clinicallycorrelated phenotypes in a largely overlapping set of HIV-positive individuals1,4,5.