Based on phenotype analyses of mutants RMgm-40 and RMgm-44 that lack expression of P36p/P52 (In this study these parasites have been used to analyse sporozoites in the skin of mice):Gliding motility, hepatocyte traversal and hepatocyte invasion in vitro (HepG2) of mutant sporozoites is similar to wild type sporozoites. Liver stage development is strongly impaired and parasites do not develop into the schizont stage and most invaded parasites cannot be detected anymore at 24 hours after infection. Inside the hepatocytes the formation of a parasitophourous vacuole is not detected at 15 and 24h after infections as shown by staining with antibodies against the parasithophorous vacuole membrane protein PbExp1 (HEP17).Infection of mice (C57BL/6) by bite of infected mosquitoes did not result in blood stage infection. Only intravenous inoculation of very high numbers of sporozoites (50.000) resulted in blood stage infection in a very low percentage of the mice.

Gliding motility is similar to wild type sporozoites. Hepatocyte traversal activity in vitro (HepG2) was higher than of wild type sporooites (~5 times higher). Hepatocyte invasion of mutant sporozoites was significantly decreased (~8% of that of wildtype). 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 strongly reduced (3000 times compared to wildtype).

Gliding motility, hepatocyte traversal and hepatocyte invasion in vitro (HepG2) of mutant sporozoites is similar to wild type sporozoites. Liver stage development is strongly impaired and parasites do not develop into the schizont stage and most invaded parasites cannot be detected anymore at 24 hours after infection. Inside the hepatocytes the formation of a parasitophourous vacuole is not detected at 15 and 24h after infections as shown by staining with antibodies against the parasithophorous vacuole membrane protein PbExp1 (HEP17).Infection of mice (C57BL/6) by bite of infected mosquitoes did not result in blood stage infection. Only intraveneous inoculation of very high numbers of sporozoites (50.000) resulted in blood stage infection in a very low percentage of the mice.

Gliding motility, hepatocyte traversal and hepatocyte invasion in vitro (HepG2) of mutant sporozoites is similar to wild type sporozoites. Liver stage development is strongly impaired and parasites do not develop into the schizont stage and most invaded parasites cannot be detected anymore at 24 hours after infection. Inside the hepatocytes the formation of a parasitophourous vacuole is not detected at 15 and 24h after infections as shown by staining with antibodies against the parasithophorous vacuole membrane protein PbExp1 (HEP17).Infection of mice (C57BL/6) by bite of infected mosquitoes did not result in blood stage infection. Only intraveneous inoculation of very high numbers of sporozoites (50.000) resulted in blood stage infection in a very low percentage of the mice.