Receptor for a number of inflammatory CC-chemokines including CCL3/MIP-1-alpha, CCL4/MIP-1-beta and RANTES and subsequently transduces a signal by increasing the intracellular calcium ion level. May play a role in the control of granulocytic lineage proliferation or differentiation. Participates in T-lymphocyte migration to the infection site by acting as a chemotactic receptor (PubMed:30713770). (Microbial infection) Acts as a coreceptor (CD4 being the primary receptor) of human immunodeficiency virus-1/HIV-1. Interacts with PRAF2 (PubMed:15757671). Efficient ligand binding to CCL3/MIP-1alpha and CCL4/MIP-1beta requires sulfation, O-glycosylation and sialic acid modifications. Glycosylation on Ser-6 is required for efficient binding of CCL4 (PubMed:11733580, PubMed:8663314, PubMed:8699119, PubMed:10383387). Interacts with GRK2 (PubMed:10085131). Interacts with ARRB1 and ARRB2 (PubMed:11448957, PubMed:16144840). Interacts with CNIH4 (PubMed:24405750). Interacts with S100A4; this interaction stimulates T-lymphocyte chemotaxis (PubMed:30713770). (Microbial infection) Interacts with HIV-1 surface protein gp120. (Microbial infection) May interact with human cytomegalovirus/HHV-5 protein UL78. Highly expressed in spleen, thymus, in the myeloid cell line THP-1, in the promyeloblastic cell line KG-1a and on CD4+ and CD8+ T-cells. Medium levels in peripheral blood leukocytes and in small intestine. Low levels in ovary and lung. (Microbial infection) May be down-regulated by human cytomegalovirus/HHV-5 protein UL78. Sulfated on at least 2 of the N-terminal tyrosines. Sulfation contributes to the efficiency of HIV-1 entry and is required for efficient binding of the chemokines, CCL3 and CCL4. O-glycosylated, but not N-glycosylated. Ser-6 appears to be the major site even if Ser-7 may be also O-glycosylated. Also sialylated glycans present which contribute to chemokine binding. Thr-16 and Ser-17 may also be glycosylated and, if so, with small moieties such as a T-antigen. Palmitoylation in the C-terminal is important for cell surface expression, and to a lesser extent, for HIV entry. Phosphorylation on serine residues in the C-terminal is stimulated by binding CC chemokines especially by APO-RANTES. Variations in CCR5 are associated with resistance or susceptibility to immunodeficiency virus type 1 (resistance or susceptibility to HIV-1) [MIM:609423]. Variations in CCR5 gene also influence the rate of progression to AIDS after infection. Ser-60 variant, a naturally occurring mutation in a conserved residue in the first intracellular domain of CCR5, results in reduced amounts of the protein in the membrane and consequently may be associated with reduced susceptibility to infection by microbes that depend on these molecules as their receptors. Variations in CCR5 are associated with susceptibility to West Nile virus (WNV) infection [MIM:610379]. Disease susceptibility is associated with variants affecting the gene represented in this entry. Belongs to the G-protein coupled receptor 1 family. CC chemokine receptors entry CCR5 receptor entry