Blocked hepatic-stage parasites and decreased susceptibility to Plasmodium berghei infections in BALB/c mice.

The BALB/c strain of mice is comparatively more resistant to sporozoite infections of Plasmodium berghei than the C57BL6 strain. Infection with live sporozoites results in the formation of small hepatic forms in the BALB/c liver that persist for as long as 6 days. Upon infection with small numbers of sporozoites, some of the parasites are destroyed in the liver whereas the rest persist as blocked forms. When larger numbers of sporozoites are injected the same process occurs but, in addition, a fraction of the liver-stage parasites complete full development and give rise to blood forms. Although blocked liver forms persist until day 6 post-infection they actually develop to only 24 h of maturity. The nature of these persistent forms is similar to those obtained from irradiated sporozoite immunization. There is a stronger cell proliferation to liver-stage antigens by spleen lymphocytes of irradiated sporozoite-immunized BALB/c mice in comparison to that of immunized C57BL6 mice suggesting that a stronger priming to liver-stage antigens, probably due to the presence of blocked hepatic forms in the liver for a longer period of time (as compared to C57BL6), occurs in the BALB/c mice. This could be a reason for the long-lasting protective memory observed in BALB/c mice.