Once upon a time, deep within a human liver lurked a dark and malign force. It was called Plasmodium!
Weeks ago, the epidermal layer of a young human had been pierced, anaesthetic injected and a certain amount of blood siphoned off, satisfying the breakfast requirements of a particular female mosquito, Anopheles by name.
From Anopheles’ point of view, the operation had been a success. The discomfort to the human was minimal—a little scratching didn’t seem much to put up with for supporting such a worthy cause.
But in the scuffle, Plasmodium had snuck by unnoticed, escaping from the digestive tract of Anopheles where he had completed the first phase of his life cycle. Slithering through Anopheles’ profound proboscis, Plasmodium paddled from capillary to vein to artery, finally coming to rest there in Human’s liver where the climate seemed right for setting up house.
Now Plasmodium multiplied. He shuffled his progeny into red corpuscles passing through the liver. He planned to send them out in great swarms and flocks; back into Human’s blood stream, causing fevers and perhaps even death to his host, all in the hope of a second coming of Anopheles or one of her cousins. Then the fortunate progeny would re-enter the mosquito’s proboscis and head back to its intestine to complete the plasmodium life cycle.
That was the plan. Then Plasmodium met the Sickle Cell.
The Sickle Cell was a red corpuscle but unlike any other corpuscle Plasmodium had ever encountered. The Sickle Cell was the product of a mutant gene. It was scaly, thick-skinned and of course, sickle shaped. Despite his best efforts Plasmodium found himself unable to penetrate the mutant cell with any consistency. His progeny could not enter the cell, his life cycle was abbreviated. If there was a second coming, this particular plasmodium would not be there for its arrival.
And Human (who it appeared was no ordinary human) escaped with only a mild fever before his immune system had thoroughly routed Plasmodium and the malaria it caused. So the young human survived malaria and with the help of his sickle-celled benefactor he passed through puberty and went on to procreate, passing on the potential for his sickle cell attribute, via one mutant gene to his children.
But after extending Human’s life another few years, the Sickle Cell finally atrophied and the same horny, scaly sickle-shaped exterior which had rejected Plasmodium, now caused the red corpuscles to clog Human’s capillaries like a log jam, restricting the blood supply to vital organs. Human, who was inhabited by a large population of these sickle cells, grew anemic and himself finally died, the victim of Sickle Cell Anemia, a genetic condition based on the presence of that one gene.
* * *
Thousands of years ago in equatorial regions of North Africa, malaria was a significant mortality factor. Those individuals without the sickle cell attribute tended to succumb to malaria at a fairly young age, often before child bearing. Those with the gene for the sickle cell however usually survived the malaria, finally succumbing to Sickle Cell Anemia in their twenties or thirties—well into reproductive age.
So in areas where malaria was prevalent, those with the sickle-cell gene were selected by nature for their resistance to that threat even greater than early personal demise: genocide—the end of a genetic lineage.
But for a moment think of the enlightened self-interest exhibited by our storied gene, determining the demise of an individual in return for the continuation of a species. Might this be a demonstration of a rudimentary form of self sacrifice, the beginnings of altruistic cooperation?
Imagine the makings of a moral system imprinted deep within a human cell!
Could an entity as simple as a gene—to us almost an abstraction—exhibit the transcendental attributes we reserve exclusively for our saints and martyrs?
Perhaps our chromosomal chain carries a link for altruism.
Genes mutate while populations evolve, and just like all other creatures, humans put their genes on one leg at a time.