There are several mechanisms responsible for the extensive antigenic diversity found in the asexual blood stages of Plasmodium falciparum. Failure to express antigens is a feature of many isolates cultured in vitro but probably is not a major cause of antigenic diversity in vivo. Numerous point mutations occur in allelic forms of asexual blood stage antigens and are assumed to contribute to antigenic diversity but as yet few such mutations have been mapped to antigenic epitopes. A major cause of antigenic diversity is the expression of different repetitive sequences in allelic forms of several antigens including the S-antigen and the two merozoite surface antigens, MSA-1 and MSA-2. The sequencing data indicates that S-antigen genes fall into many allelic families whereas both MSA-1 and MSA-2 are dimorphic. Further diversity has arisen as a result of intragenic recombinations between the dimorphic forms of both MSA-1 and MSA-2. In addition to this diversity reflecting the expression of different allelic genes, asexual blood stages of malaria parasites undergo antigenic variation in that clonal parasite populations can vary the form of an antigen on the surface of infected erythrocytes. Antibodies or DNA probes directed against variable repeat sequences can be used to distinguish different isolates of P. falciparum. The use of antibodies to S-antigen repeats has been particularly useful for typing the parasites causing infections. The application of S-antigen typing to field studies in Papua New Guinea has demonstrated marked diversity in the parasites causing infections in one area.