Streptococcus agalactiae also named Group B Streptococcus (GBS) is the most significant pathogen causing invasive infections, such as bacteremia and meningitis in neonates. Worldwide epidemiological studies have shown that a particular clonal complex (CC) of capsular serotype III, the CC17, is strongly associated with meningitis in neonates and is therefore designated as the hypervirulent clone. Macrophages are a permissive niche for intracellular bacteria of all GBS clones. In this study we deciphered the specific interaction of GBS CC17 strains with macrophages. Our study reveals that CC17 strains are phagocytosed at a higher rate than GBS non-CC17 strains by human monocytes and macrophages in cellular models and primary cells. CC17 hyper-phagocytosis is preceded by an initial hyper-attachment step to macrophages mediated by the PI-2b pilus (Spb1) and the CC17 specific HvgA surface protein. We showed that two different inhibitors of scavenger receptors (fucoidan and poly(I)) specifically inhibited CC17 phagocytosis while they did not affect non-CC17 phagocytosis. Once phagocytosed, both CC17 and non-CC17 strains remain in a LAMP-1 positive vacuole that ultimately fuses with lysosomes, and their survival within macrophages is similar. Bothe strains display a basal egress which occurs independently from actin and microtubules networks. Our findings provide new insights into the interplay between the hypervirulent GBS CC17 and major players of host innate immune response. This enhanced phagocytosis could reflect a peculiar capacity of CC17 lineage to subvert the host immune defense and establish a niche for intracellular persistence.