After an initial brief period of cross-reactive neutralization, possibly due to the high maternal antibody titer that co-ligates the inhibitory FcγRIIB [38], the virus-antibodies complexes facilitated infection of myeloid cells, such as monocytes, through activating Fc-R to result in increased virus replication and output [16]–[18]. This evidence concerns the gene FCGR2B and infection.