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Low CCR5 expression protects HIV-specific CD4+ T cells of elite controllers from viral entry

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Claireaux, Mathieu | Robinot, Rémy | Kervevan, Jérôme | Patgaonkar, Mandar | Staropoli, Isabelle | Brelot, Anne | Nouël, Alexandre | Gellenoncourt, Stacy | Tang, Xian | Héry, Mélanie | Volant, Stevenn | Perthame, Emeline | Avettand-Fenoël, Véronique | Buchrieser, Julian | Cokelaer, Thomas | Bouchier, Christiane | Ma, Laurence | Boufassa, Faroudy | Hendou, Samia | Libri, Valentina | Hasan, Milena | Zucman, David | de Truchis, Pierre | Schwartz, Olivier | Lambotte, Olivier | Chakrabarti, Lisa, A.

Edité par CCSD ; Nature Publishing Group -

International audience. HIV elite controllers maintain a population of CD4 + T cells endowed with high avidity for Gag antigens and potent effector functions. How these HIV-specific cells avoid infection and depletion upon encounter with the virus remains incompletely understood. Ex vivo characterization of single Gag-specific CD4 + T cells reveals an advanced Th1 differentiation pattern in controllers, except for the CCR5 marker, which is downregulated compared to specific cells of treated patients. Accordingly, controller specific CD4 + T cells show decreased susceptibility to CCR5-dependent HIV entry. Two controllers carried biallelic mutations impairing CCR5 surface expression, indicating that in rare cases CCR5 downregulation can have a direct genetic cause. Increased expression of β-chemokine ligands upon high-avidity antigen/TCR interactions contributes to autocrine CCR5 downregulation in controllers without CCR5 mutations. These findings suggest that genetic and functional regulation of the primary HIV coreceptor CCR5 play a key role in promoting natural HIV control.

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