GBP2 and infection: Infection of wildtype and GbpChr3-KO mice with wildtype or fusion-defective B. thailandensis vgrG5ΔCTD further substantiated our hypothesis that increased cell-cell fusion, bacterial replication, and VgrG5-induced pathology contribute to the susceptibility of GBP-deficient mice (Fig 6D). Histological analysis of infection in wildtype and Gbp2−/− mice with wildtype B. thailandensis or B. thailandensis vgrG5ΔCTD (5 x 103) showed that the increased pathology and bacterial replication observed in Gbp2−/− mice requires the VgrG5 CTD (Fig 6E and 6F, S6A and S6B Fig).