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    Defense against HIV-1: a new protective function of IgA reported

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    A study directed by Morgane Bomsel

    Upon sexual human immunodeficiency virus type-1 (HIV-1) infection, anti-viral type A immunoglobulins (IgA)are produced in the genital mucosa.

    By which mechanisms do IgAs  fight against HIV-1? In this study, Morgane Bomsel's team identifies a new IgA protective function, namely their ability to trigger HIV-1 infected cells lysis in turn blocking HIV-1 transmission. These results highlight the importance of assessing this new IgA anti-viral activity in the evaluation of vaccine efficacy as well as in diagnosis of recent HIV-1 infection. Moreover, this IgA property could be exploited to eradicate persistent viral reservoirs in HIV-infected people under effective anti-retroviral therapy. These results are published on march 29th,  2018 in Frontiers in Immunology.

    HIV-1 transmission largely occurs through genital mucosal epithelium during sexual intercourses. Morgane Bomsel's team focus her research on the mucosal immune response developed locally at the level of the genital mucosa during HIV-1 infection. Indeed, deciphering these defense mechanisms can provide solid grounds to develop strategies to block sexual transmission of HIV-1 but also to evaluate the efficacy of an HIV-1 vaccine approach. In the genital mucosa, two families of antibodies protect against HIV-1: locally produced type A immunoglobulins, IgA and type G immunoglobulins, IgG circulating in the blood. These two families of antibodies exert several anti-viral functions including the ability to neutralize the virus. IgA also blocks the transport of the virus through the mucosa by a phenomenon referred to as transcytosis, and IgG mediate the lyse of HIV-infected CD4+ T cell.

    In this new study, Morgane Bomsel's team highlighted an additional anti-viral IgA property unknown so far: the capacity to mediate HIV-1 infected CD4 +T cells lysis, in a mechanism similar to that of IgG. In addition, the authors show that IgA and IgG cooperate to increase efficient lysis of HIV-1 infected cells.

    These results have major clinical implications for several reasons. On the one hand, they reveal the importance of assessing the lytic activities of IgA, IgG and their combination for a full evaluation of the efficacy of a vaccine. On the other hand, because such lytic antibodies are produced very early upon HIV-1 infection, the respective measurement of lytic IgA and IgG-mediated activities alone or in cooperation could improve the sensitivity of HIV-1 diagnosis in recent infection. Finally, the cooperative lytic properties of IgA and IgG could be exploited to eradicate persistent viral reservoirs in HIV-1-infected patients on effective anti-retroviral therapy.

     

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