Ovalocytosis without band 3 gene 27-bp deletion and malaria infection

Genetic adaptation to malaria is a longstanding research topic in anthropology and human genetics. Southeast Asian ovalocytosis (SAO) has been documented to have resistance to malaria; however, the implications of existing data are controversial. In particular, SAO resistance to malaria is unlcear in terms of the types of SAO, with/without the 27-base pair deletion in the band 3 gene (B3Δ27). To shed light on the relationships between SAO and malaria, we surveyed Plasmodium infection, erythrocyte morphology, and the presence of the B3Δ27 among the residents of a selected area in East Kalimantan, Indonesia where malaria is endemic. We screened peripheral blood smears (n = 128) for Plasmodium infection and erythrocyte morphology under a microscope, and then DNA was extracted from the smears to be used as a template for a polymerase chain reaction to detect the B3Δ27. The prevalence of infection with Plasmodium including Plasmodium vivax and Plasmodium falciparum was approximately 30%. Among a total of 128 subjects, 9.4% and 18.0% showed moderate (ovalocytic cells: 30–49%) and severe (ovalocytic cells: 50–100%) ovalocytosis, respectively. A total of three B3Δ27 carriers were identified. The data set was statistically analyzed and we observed that (1) higher ovalocytic rate resulted in lower malaria infection and (2) the B3Δ27 did not prevent malaria infection. These results suggest that resistance of SAO to malaria is due to SAO without the B3Δ27

Biology · Gene · Malaria · Parasite hosting · Plasmodium (life cycle · Plasmodium falciparum · Plasmodium vivax · Polymerase chain reaction · Erythrocyte Function and Pathophysiology · Hemoglobinopathies and Related Disorders · Malaria Research and Control · Genetics · Immunology · Virology