Roughly300,000 childrenare born with sickle cell disease ( SCD ) , otherwise known as sickle electric cell anaemia , every class and it is thought that250 million peopleworldwide carry the cistron creditworthy .

The experimental condition affect the shape of the normally round red-faced ancestry cellular telephone , change state them crescent or sickle - like . This   can cause the blood to clot , resulting in infection and severe blood loss . Those with the most severe form of the disease often do n’t make it past their fifth birthday .

Now , scientists believe that this widespread , often deadly condition is the resultant of just one genetic mutant that occurred a piffling over 250 generations ago .

The sketch , published in theAmerican Journal of Human Geneticslast week , was carried out by a squad of research worker at the Center for Research on Genomics and Global Health , an offshoot of the National Institute of Health ( NIH ) .

Using historic records and analysis of the genome of tightlipped to 3,000 people with some genetical account of the disease , the researchers were able to nail the most probable clock time and place of its source : TheGreen Sahara7,300 years ago , which makes it roughly 259 coevals old . However , they add that it may have originated somewhere in West - Central Africa .

At about this time , a child would have been born with a genetic genetic mutation in one chromosome , dissemble the shape of the blood ’s hemoglobin . The kid would n’t have support because the other cistron would have been perfectly normal , but he or she would have grown up and had children of his or her own , thus passing on the gene to the next generation .

The genetic mutation would have endure , passing on for one C of geezerhood before one unfortunate child   would have   been conduct with two copies of the variation and , therefore , have developed sickle cubicle anaemia .   The first immortalize cases in history take place in Egypt during the predynastic period ( 3200 BCE ) .

During the Bantu migrations and , later , the slave craft , SCD would have journey to other constituent of Africa and to other parts of the earth , let in the Near East , India , and Southern Europe , grow into dissimilar pigboat - type along the way .

In most cases , a virulent genetic mutation like this would not live , but the sickle cell mutation has because it comes with an important genetic advantage . One affected chromosome can protect its carrier against malaria   –   it is not a coincidence that reaping hook cell is far more prevalent in countries at a high risk of infection of malaria . It appears SCD efficaciously starve the leech responsible for malaria because it can not feed on the reap hook - regulate cells .

The scientists involved in the sketch hope this inquiry can help meliorate aesculapian care for people with SCD , provide medics a direction to better foretell   whether a patient will develop a severe or mild form of the disease .