Abstract

R. K. Obi*, C. C. Okangba, F. C. Nwanebu, U. U. Ndubuisi and N. M. Orji

Malaria parasites have evolved to maintain a well-balanced relationship with their human hosts. This implies that they can partially escape from protective effector mechanisms of their hosts, but also that hosts can develop partial immunity to the parasite. This immunity requires repeated infections, takes years to develop and is usually of short duration. However, protective immunity to clinical malaria rather than infection may be of long duration. This natural acquired immunity is called premunition since a low parasitemia mostly persists in the presence of circulating antibodies to the various stages and in the absence of clinical disease. In children who do not have circulating antibodies to the parasite, premunition is probably caused by antitoxic immunity. These poor and slowly developing immune responses to malaria are partly due to immune evasion strategies of the parasite caused by antigenic polymorphism, shedding of parts of parasite proteins, cross-reactive epitopes of antigens of different developmental stages, prolonged exposure to endemic malaria and widespread restricted immunogenicity to defined antigens. Premunition relies on the cooperation between the parasite and human antibodies, leading to the induction of antibody dependent cellular inhibition (ADCI) of the intra-erythrocytic growth of the parasite. The immunity, however, is not a sterilizing type in that the infection persists longer than the symptoms and individuals can exhibit relapses or recrudescences or become reinfected.