Fig. 1.

Shared antigens between liver and blood-stage malaria parasites can induce cross-stage immunity.

Malaria infection is initiated by an infectious mosquito bite, which inoculates a few sporozoites into the skin. Sporozoites then migrate to the liver and invade hepatocytes. During pre-erythrocytic development (which last 7 days for Plasmodium falciparum) parasite load slowly increases as Plasmodium matures in the liver. In addition, the antigenic repertoire becomes increasingly similar to blood-stage parasites [9] and cross-stage antigens are expressed. Late liver schizonts contain up to 40,000 merozoites [18], which are released into the blood-stream as merosomes surrounded by a host cell membrane [53]. When each merozoite invades an individual red blood cell parasite load rises rapidly. Blood-stage parasites mature from rings to trophozoites and schizonts and parasite load increases exponentially with each new replication cycle (P. falciparumtakes 48h to complete one blood-stage cycle). Apart from typical blood-stage antigens infected erythrocytes also express cross-stage antigens, which are shared with pre-erythrocytic parasites. There is evidence from subunit and whole parasite immunization approaches that shared antigens between pre-erythrocytic and blood-stage parasites could induce cross-stage immunity. Characterization of these antigens would greatly facilitate multi-stage malaria vaccine development.