CCR6 ligands inhibit HIV by inducing APOBEC3G

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Abstract
We have identified a postentry CCR6-dependent mechanism of inhibition of HIV occurring at an early stage of infection mediated by the induction of the host restriction factor apolipoprotein B mRNA-editing enzyme-catalytic polypeptide-like 3G (APOBEC3G). We observed induction of APOBEC3G expression only in CCR6+ cells but not in cells treated with the G inhibitory (Gi) pathway inhibitor pertussis toxin. CCR6 is highly expressed on peripheral blood CD4+CCR5+ memory T cells and by 2 populations of CD4+ T cells within the gut, α4β7+ and T helper type 17, that have been implicated in cell-to-cell spread of HIV and enhanced restoration of CD4+ T cells within gut-associated lymphoid tissue, respectively. This novel CCR6-mediated mechanism of inhibition allows the identification of pathways that induce intrinsic immunity to HIV, which could be useful in devising novel therapeutics that selectively target CCR6+ cells.