摘要：来自德国汉堡的BNITM以及加纳Kumasi 大学的研究人员发现了一种人类遗传变异，会将患严重疟疾的风险降低30%，在儿童疟疾患者中FAS位点的变异可以阻止过多的有潜在风险的免疫反应。
The study appears in the open-access journal PLoS Genetics on May 19.
Severe malaria is a major public health burden in Sub-Saharan Africa, where approximately one million individuals die each year as a result of infection with Plasmodium falciparum. Whereas adults in endemic areas develop some resistance to malaria, preventing severe complications, children under the age of five years can develop life-threatening forms of the disease. To date, the molecular mechanisms causing these manifestations are poorly understood.
FAS encodes for CD95, a molecule critically involved in the programmed death of some white blood cells. This candidate gene study, including more than 6,000 child subjects, details how a single nucleotide variant of FAS predisposes its carriers to a higher number of immune cells prone to suicide. These findings indicate that a genetic predisposition to an increased expression of CD95 may help to protect from severe malaria, possibly by rendering a type of white blood cell more susceptible to programmed cell death.
Kathrin Schuldt, co-author, said, "We believe that our study will help to unravel the mechanisms causing the fatal forms of malaria."
