Sickle Cell Anaemia and Malaria
Researchers discover how carriers of the sickle-cell anaemia gene are protected from malaria. Teasing out the mechanism which helps people with one sickle-cell gene even carrying one copy of it confers some resistance to malaria. Sickle Cell Trait (SCT) has been shown to be protective against malaria. A growing literature suggests that malaria exposure can reduce.
Relationships between sickle cell trait, malaria, and educational outcomes in Tanzania
First, one type of malaria, that caused by Plasmodium falciparum, is highly lethal. Second, it is estimated to have been around in many parts of the world for several thousands of years, i. Third, deaths from malaria take place mostly in children, i.
Last but not least, Plasmodia take on different forms in the course of their life cycle, but what causes disease are the intra-erythrocytic parasites: Balanced Polymorphism Many fundamental experiments in genetics have been carried out in micro-organisms, and biological selection is a good example. Growing bacteria in a culture medium containing streptomycin is a very simple and certain way to select for the few bacteria, within the culture, that already had a gene — we can call it strr — that makes them resistant to this antibiotic.
How Sickle Cell Protects Against Malaria? - Scientific Animations
If we now isolate one of the resistant bacteria we can grow up a new culture in which the entire population will be streptomycin resistant. It happens that the streptomycin-resistant bacteria do not grow quite as fast as the streptomycin-sensitive ones: Since bacteria are mostly haploid i.
Since we humans, like most animals, are diploid, we have in this respect more options. Several studies suggested that, in one way or another, sickle hemoglobin might get in the way of the Plasmodium parasite infecting red blood cells, reducing the number of parasites that actually infect the host and thus conferring some protection against the disease.
The IGC team's results challenge this explanation.
In painstakingly detailed work, Ana Ferreira, a post-doctoral researcher in Miguel Soares' laboratory, demonstrated that mice obtained from Prof. Yves Beuzard's laboratory, that had been genetically engineered to produce one copy of sickle hemoglobin similar to sickle cell trait, do not succumb to cerebral malaria, thus reproducing what happens in humans.
- Sickle Cell Anaemia and Malaria
- Protective Effect of Sickle Cell Trait Against Malaria-Associated Mortality And Morbidity
- Relationships between sickle cell trait, malaria, and educational outcomes in Tanzania
Ingo Bechman observed the brains of these mice he confirmed that the lesions associated with the development of cerebral malaria where absent, despite the presence of the parasite.
Ana Ferreira went on to show that the protection afforded by sickle hemoglobin in these mice, acts without interfering directly with the parasite's ability to infect the host red blood cells. As Miguel Soares describes it, "sickle hemoglobin makes the host tolerant to the parasite".
Through a series of genetic experiments, Ana Ferreira was able to show that the main player in this protective effect is heme oxygenase-1 HO-1an enzyme whose expression is strongly induced by sickle hemoglobin. The genetic variations generated by SCD provide an opportunity to identify the effect of malaria exposure in childhood on educational attainment.
Using the technique of Mendelian randomization, the key assumption is that a specific genotype in this case HbAS is linked to a health-related characteristic protection from malariabut is unrelated to other confounding variables or to the outcome of interest [ 13 ]. If this assumption is valid, then individuals with SCT will have reduced exposure to malaria but will otherwise be comparable to individuals without sickle cell trait. This property of SCT has been previously used, in a Mendelian randomization framework, to study the relationship between malaria and stunting [ 14 ], but has not to our knowledge been used to study the relationship between malaria and educational attainment.
Methods Study area The data used in this study was collected in Korogwe district in north-eastern Tanzania. The district is characterized by varying malaria transmission with areas in the lowlands having high transmission, where Plasmodium falciparum is the dominant malaria species [ 1516 ].
Out of 14 villages, six have been participating in surveillance of febrile episodes using community health workers known as community owned resource persons CORPs [ 18 ]. Two of these villages Kwamasimba and Mkokola started the passive case detection PCD of febrile episodes in [ 19 ], while in the remaining four villages the surveillance was introduced in January Over 30, febrile illnesses have been recorded from the six villages since January Data from the HDSS shows that bythe number of households in the six villages in which PCD of fever was operational waswith a total population of 14, people.
Genotyping was done by the MalariaGEN genomic epidemiology network. Educational attainment information was obtained for Genotype data was collected specifically for research purposes, malaria and fever diagnosis data was collected as part of the implementation of the passive case detection system of febrile illness, and education and other socioeconomic status indicators were collected through the routine procedures of the Korogwe Health and Demographic Surveillance System.
Permission was obtained to use the data for this study.SICKLE CELL TRAIT RESISTS MALARIAL INFECTION
Outcome variables The primary outcome variables analyzed were a continuous measure of educational attainment, defined as highest grade of schooling attained, and a binary measure school enrolment, both measured as of Secondary outcome variables were febrile illness and malaria over the period —