Purpose of review
Recently, studies have suggested a role for Fc-mediated effector functions in viremic control of HIV infection and blocking HIV acquisition. Although progress has been made in identifying the mechanisms responsible for regulating various innate functions, minimal research has been performed concerning macrophage-specific phagocytosis and antiviral effects.
Of what research has been performed, phagocytosis has been identified as a possible key player in antiviral functions during initial infection, offering protection at the HIV mucosal entry sites. Recent research has also highlighted the importance of various antibody characteristics, such as polymorphism, immunoglobulin subclass, and glycan structure on those effector functions modulated. Lastly, despite recent failures in HIV vaccine trials, the RV144 Thai trial illustrated 31.2% efficacy against heterosexual infection. When these protective results were looked at in depth, vaccine-induced antibodies were increased when infection rates decreased, suggesting that HIV might be neutralized through receptor-mediated effector mechanisms, including phagocytosis. Importantly, these data instilled the awareness that the identification of protective immune correlates is imperative to successfully develop vaccine strategies.
In this review, we address the antiviral mechanisms of phagocytosis, focusing on complement-mediated phagocytosis and Fc-receptor-mediated antibody-dependent cellular phagocytosis in relation to HIV transmission and infection.