The case of CCR5 illuminates the risks of genetic tinkering
IT IS A good rule in matters genetic to assume that things are there for a purpose. This is not to say that the wrong sort of DNA cannot cause disease. It can. But disease-causing mutations are rare, because natural selection makes them so. Far more common are genes of pedestrian function that are somehow dismissed as dispensable.
One such is CCR5, which encodes a protein found on the surface membranes of certain types of cells, especially cells of the immune system. CCR5 is one of a group of membrane proteins called beta chemokine receptors. These are involved in inflammatory responses, but CCR5 does not seem to be essential to such responses. What is crucial about it, though, is that in the wrong circumstances it can harm the body it is in.
Comparing DNA with lifespan, and making suitable adjustments for the age-profile of those in the database being different from that of the population as a whole, Dr Wei and Dr Nielsen calculated that people who are homozygous for delta-32 CCR5 are 20% more likely than those who are not to die before the age of 76. Presumably, though this is still guesswork, delta-32 homozygosity damages the body’s immune response and gives infectious agents a helping hand.
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