To test if gp34 and gp68 suffice to impair IgG-dependent activation of FcγRs, two factors of our experimental approach were modified: (i) gp34 and gp68 were expressed outside the context of HCMV infection by recombinant vaccinia viruses, and (ii) instead of polyclonal HCMV IVIG, a well-defined humanized therapeutic monoclonal IgG1 antibody (trastuzumab) was used as an activator of host FcγRs upon binding to its antigen HER2. Here, TNFSF4 is linked to cytomegalovirus infection.