Ovalocytosis without band 3 gene 27-bp deletion and malaria infection
Ovalocytosis without band 3 gene 27-bp deletion and malaria infection
复制标题
DOI:
10.1537/ase.050802
复制
发表时间:
2006-08-01
影响因子:
0.7
通讯作者:
Ishida, Takafumi
中科院分区:
文献类型:
--
作者:
Kimura, Masako;Soemantri, Augustinus;Ishida, Takafumi
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 (B3 Delta 27). To shed light on the relationships between SAO and malaria, we surveyed Plasmodium infection, erythrocyte morphology, and the presence of the B3 Delta 27 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 B3 Delta 27. 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 B3 Delta 27 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 B3 Delta 27 did not prevent malaria infection. These results suggest that resistance of SAO to malaria is due to SAO without the B3 Delta 27.