![]() ![]() As Miguel Soares describes it, "sickle hemoglobin makes the host tolerant to the parasite." ![]() 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.Īna 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. 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. In painstakingly detailed work, Ana Ferreira, a post-doctoral researcher in Miguel Soares' laboratory, demonstrated that mice obtained from Prof. ![]() The IGC team's results challenge this explanation. 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. ![]() Despite several decades of research, the mechanism underlying this protective effect remained elusive. These findings lead to the widespread believe in the medical community that understanding the mechanism whereby sickle cell trait protects against malaria would provide critical insight into developing treatment or a possible cure for this devastating disease, responsible for over a million premature deaths in sub-Saharan Africa. However, it was found that these same individuals, said to carry the sickle cell trait, were in fact highly protected against malaria, thus explaining the high prevalence of this mutation in geographical areas where malaria is endemic. Individuals carrying just one copy of the sickle mutation (inherited from either the father or mother) were known not to develop sickle cell anemia, leading rather normal lives. Observations made during the mid-20th century and building on Pauling's findings, revealed that the sickle mutation is, in fact, highly, selected in populations from areas of the world were malaria is very frequent, with sometimes 10-40% of the population carrying this mutation. This is however, far from being the case. If untreated, these individuals have a shorter than normal life expectancy and as such it would be expected that this mutation would be rare in human populations. Only those individual that inherit two copies of the sickle mutation (one from their mother and the other from their father) develop sickle cell anemia. The cause of sickle cell anemia was attributed unequivocally to a single base substitution in the DNA sequence of the gene encoding the beta chain of hemoglobin, the protein that carries oxygen in red blood cells. It is an inherited disorder - the first ever to be attributed to a specific genetic modification (mutation), in 1949 by Linus Pauling (two-times Nobel laureate, for Chemistry in 1954, and Peace, in 1962). Sickle cell anemia is a blood disease in which red blood cells reveal an abnormal crescent (or sickle) shape when observed under a conventional microscope. ![]()
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