Rabies virus (RABV), causes a fatal encephalitis disease contributing to an estimated annual death toll of 40 000–70 000 people worldwide. Without effective therapeutic treatment, RABV has a mortality rate approaching 100%. However, it remains unclear how RABV hijack cellular factors to subvert antiviral defenses and enable virus replication. As interactions with these proteins are critical for viral infection and pathogenesis, small molecules or biologics therapies targeting these interfaces may serve as potential antiviral agents. In this study, to better understand how RABV G protein rewire the host cell, we generated a different strains RABV G proteins-human protein interaction map.