In vitro invasion of hepatocytes by the sporozoites is not affected. Liver stage development is strongly impaired. Liver stage numbers are reduced by ~50% twenty four hours after invasion of HepG2 cells. At later time points, mature liver schizonts are absent. Only developmentally arrested liver forms persist.Infection of mice (C57BL/6) by bite of infected mosquitoes or subcutaneous inoculation of sporozoites did not result in blood stage infection. Only intraveneous inoculation of very high numbers of sporozoites (50.000) resulted in blood stage infection in ~50% of the mice. These mice showed a prolonged prepatent period.

Normal, wild-type-line invasion of hepatocytes. The development of liver stages is strongly impaired after 24h.

In vitro invasion of hepatocytes by the sporozoites is not affected. Liver stage development is strongly impaired. In vivo (BALB/c mice), the number of liver stages at 2 hours after intravenous injection of sporozoites is reduced by 60%. The number of liver stages at 24h were reduced by >95%. liver stages could not be detected at 40h after infection. Liver stages were morphologically similar to wt liver stages at 6 and 12h after infection, a time when the intrahepatocytic transformation from elongate sporozoite to spherical trophozoites commences. Antibody staining for HEP17, a parasitophorous vacuole membrane (PVM)protein, showed a typical circumferential pattern, which indicates that the PVM is present. Liver stages did not develop into schizonts but appeared to be arrested at the trophozoite stage. Arrested liver stages did not persist in the liver after 40h. Infection of BALB/c mice by intravenous inoculation of high numbers of sporozoites (50.000) did not result in blood stage infection.