Normal sporozoite production. Sporozoites fail to establish an infection in hepatocytes. Analysis of the kinetics of Pbp36 sporozoite invasion by FACS, in comparison to control PbGFP sporozoites, revealed that genetic ablation of p36 abrogates sporozoite productive invasion of HepG2 (SR-BI-dependent entry pathway) and Hepa1-6 cells (CD81-dependent entry pathway)(see below for more phenotype information).

See remarks below ('Phenotype')

Gliding motility is similar to wild type sporozoites. Hepatocyte traversal activity in vitro (HepG2) was higher than of wild type sporozoites (~7 times higher). Hepatocyte invasion of mutant sporozoites was significantly decreased (~9% of that of wild type). Liver stage development is strongly impaired and parasites do not develop into the schizont stage. Infectivity of sporozoites as measured by infection of rats (Wistar) by intravenous inoculation of sporozoites was reduced (1000 times compared to wildtype).

Normal sporozoite production. Sporozoites fail to establish an infection in hepatocytes. Analysis of the kinetics of Pbp36 sporozoite invasion by FACS, in comparison to control PbGFP sporozoites, revealed that genetic ablation of p36 abrogates sporozoite productive invasion of HepG2 (SR-BI-dependent entry pathway) and Hepa1-6 cells (CD81-dependent entry pathway)(see below for more phenotype information).