CCL3L1 is a CC chemokine ligand that functions as a potent ligand for HIV co-receptor CCR5 and receptors CCR1 and CCR3 1. It exhibits chemotactic activity for lymphocytes and monocytes, with the processed form LD78-beta showing 20-30 fold higher chemotactic activity and potent HIV-1 inhibition [UniProt]. CCL3L1 operates within the chemokine-mediated signaling pathway, promoting cell migration and inflammatory responses [GO Annotations]. Mechanism: CCL3L1 functions through competitive binding to CCR5, blocking HIV-1 entry 1. The gene exhibits complex copy number variation (0-11 copies in European populations), localized to a segmental duplication hotspot on chromosome 17.2 1. Increased CCL3L1 expression enhances glioblastoma cell proliferation through CCR3 and CCR5 signaling 2. Disease Relevance: Lower CCL3L1 copy number associates with increased HIV-1 acquisition risk and faster AIDS progression 1. Copy number variation influences systemic lupus erythematosus (SLE) susceptibility and lupus nephritis severity 3. CCL3L1 expression is significantly upregulated in COPD monocyte/macrophages 4. However, CCL3L1 copy number shows no association with lung function variation 5 and limited utility for HIV-associated neurocognitive disorder prediction 6. Clinical Significance: CCL3L1 represents a promising pharmacological target; CCR5 antagonists like maraviroc show HIV suppression potential, though respiratory disease applications show limited promise 5.