Above is a graphic of the CCR5 molecule showing the general orientation in the membrane. Sites recognized by two monoclonal antibodies (PA12 and 2D7) are shown, as is the truncation point caused by the delta 32 mutation. Additional information includes mutations that block activity as a chemokine receptor but preserve function as an HIV receptor (C-terminal truncation or mutations that impact phosphorylation). Sulfation of tyrosine on the exposed N-terminal domain is required for HIV-1 infection, but is dispensable for chemokine signaling.