Antibody effector functions are mediated by binding of the IgG Fc domain to FcγRs on myeloid cells or to components of the complement system. These activities occur when the antibody binds the target virus protein either on virions or on infected cells. a, Viral particles are internalized and degraded and local cytokine release recruits immune cells. b, If cells are permissive, progeny virions could be produced. When virus–antibody complexes are taken up by the cell, a detrimental cytokine response may be generated. c, Binding of the IgG Fc fragment to C1q leads the activation of complement components C3, C3a and C5a and of the complement membrane attack complex (MAC) that disrupts membranes. C3 and C5a facilitate phagocytosis by myeloid cells. C3a and C5a are anaphylatoxins that attract inflammatory cells, which can secrete cytokines that enhance antiviral immunity but could be detrimental if produced in excess. d, e, The IgG Fc domain binds to multiple types of FcγRs on myeloid cells to trigger effector functions. The specific consequences of this interaction are dependent on the FcγR that is involved and are not detailed here. d, Antibody-dependent phagocytosis by macrophages and dendritic cells. e, Antibody-dependent cytotoxicity mediated by natural killer (NK) cells. f, Antibody-mediated antigen presentation after the uptake of virus or virus-infected cells by phagocytic cells leads to the activation of antiviral T cells.