Parasitemia develops slower in mice infected with the mutant parasites. Peak parasitemias in mice are comparable to those in wild type infected mice. More then 80% of mice infected with mutant parasites survive infection and clear the parasites from the blood.

Normal numbers of ookinetes are produced. A strong reduction in oocyst production.

A strong reduction in oocyst production (mean number of oocysts in wild type ranging from 79-213 and in mutants 3-124). Subsequent development of mutant oocysts appears to be normal. The number of mutant sporozoites in oocysts was similar to wild-type oocysts.

A strong reduction in oocyst production (mean number of oocysts in wild type ranging from 79-213 and in mutants 3-124). Subsequent development of mutant oocysts appears to be normal. The number of mutant sporozoites in oocysts was similar to wild-type oocysts. No differences of salivary gland invasion of the mutant sporozoites could be detected. Salivary gland sporozoites showed normal gliding motility. The efficiency of liver infection in vivo of the mutant sporozoites was lower (68%) compared to wild type sporozoites.

Liver-stage development was reduced as shown by a 1-day extension of the prepatent period in mice following the inoculation with 10(4) purified sporozoites. While gliding motility and the rate of cell traversal of sporozoites were similar to wild type parasites, in two out of three experiments a reduction in sporozoite in vitro invasion rates was observed that could explain (in part) the delay in the prepatent period. Immunofluorescence analyses of liver stage parasites stained with antibodies against markers for parasite development (HSP70), PVM (UIS4 and EXP1) and merozoite formation (MSP1), revealed no distinct differences in morphology and size between rom1 and wild type liver stages at 24h or 48h after sporozoite invasion.

The efficiency of liver infection in vivo of the mutant sporozoites was lower (68%) compared to wild type sporozoites.

Liver-stage development was reduced as shown by a 1-day extension of the prepatent period in mice following the inoculation with 10(4) purified sporozoites.While gliding motility and the rate of cell traversal of sporozoites were similar to wild type parasites, in two out of three experiments a reduction in sporozoite in vitro invasion rates was observed that could explain (in part) the delay in the prepatent period. Immunofluorescence analyses of liver stage parasites stained with antibodies against markers for parasite development (HSP70), PVM (UIS4 and EXP1) and merozoite formation (MSP1), revealed no distinct differences in morphology and size between rom1 and wild type liver stages at 24h or 48h after sporozoite invasion.

Analysis of course of blood stage infection in BALB/c mice indicates a mild attenuation of mutant parasites with a decrease in peak parasitemia (25% versus 43%) and a decrease in the duration of infection compared to the wildtype control

Sporozoites showed normal motility and traversal and invasion of hepatocytes. However, during development of the liver stages, the number of infected hepatocytes significantly decreased during the first 24 hours compared to wild type liver stages.