Project

Despite the success of anti-retroviral therapy (ART) to treat HIV-1-infected individuals, the persistence of a viral reservoir remains an obstacle to a cure. Characterization of the antibody repertoire in patients led to the identification of broadly neutralizing antibodies (bNAbs) targeting the viral envelope glycoproteins and suppressing HIV-1 infectivity with unprecedented potency. Passive administration of bNAbs in animal models or in infected humans revealed their capacity to decrease viral loads and to delay viral rebound after ART cessation. bNAbs also activate the immune system and mediate functions that go well beyond neutralization, such as killing of infected cells or enhancement of T and B cell responses. Immune cells with cytotoxic, phagocytic or immunomodulatory activities express Fc Receptors (FcR) that recognize the constant Fc region of antibodies. The complement cascade is also initiated through binding to the Fc. The molecular and cellular mechanisms underlying the activation of Fc-dependent effector functions of antibodies, including bNAbs, are incompletely understood. Our aim is to analyze the interactions between HIV-1 specific antibodies, infected cells, and the immune system