The Fever: How Malaria Has Ruled Humankind for 500,000 Years Read Online Free PDF Page B

antigens, the proteins that alert the immune system to launch an attack. The progeny can control the variable expression of these genes, so that when they bombard the body, each cloned parasite looks different to the immune system. Some portion may be recognized and destroyed, but those in the most novel disguises are not, and with the immune system fooled, they are able to burrow into blood cells, victorious. 48
    After thousands of years of malarial respite,
Plasmodium
was back, in its most terrifying, ferocious incarnation of all.
    Plasmodium falciparum
’s toll on early rain-forest villages would have been devastating, with both adults and children felled by the dozens, their parasite-infested blood curdled in their veins. We know of the parasite’s bloodshed some four thousand years ago because of the calamitous genetic adaptations that arose and spread.
    A single-point mutation on a single gene turns pliable blood cells into rigid, frozen crescents called sickle cells. A newborn endowed with two copies of this sickle-cell gene, before the advent of modern medicine, would not have survived childhood. But those endowed with a single dose of the sickle-cell gene—the so-called heterozygotes—found themselves with a useful weapon against the scourge that stalked them. When
P. falciparum
invaded their bloodstreams and started taking down oxygen-sucking hemoglobin, the rising level of unhitched oxygen would trigger a switch. The hemoglobin molecules in their blood cells fused together like two magnets, turninginto stiff crescents, and slashing the risk of death from
P. falciparum
by 90 percent. 49
    If two such sickle-cell gene carriers started a family together, the probability of their children being born with the uniformly fatal condition of a double dose of the sickle-cell gene ran to one in four. Even with those terrible odds, the carriers of the sickle-cell gene out-reproduced those without the gene.
Plasmodium falciparum
was so deadly that it was better to risk a 25 percent probability of a dead child than to forsake the possibility of a weapon against the parasite. 50 And so the sickle-cell gene spread throughout the five continents, lurking inside up to 40 percent of the population in parts of Africa, South Asia, and the Middle East to this day, a silent reminder of falciparum malaria’s deadly legacy and the mortal risks that surviving it has required. 51
    Humankind devised a few other weapons against
P. falciparum
. With each bout of fever, our immune systems can arduously prime themselves against yet another of the parasite’s multifarious disguises. The more infections we suffer, the savvier to
P. falciparum
’s antigenic guises our immune systems become, which allows people with multiple exposures to enjoy a modicum of immunity to the parasite. They still get infected, but with their immune systems restraining the parasites’ numbers to as much as one million times lower than in those not immune, they may not get as sick. They will almost certainly not die. 52
    But such immunity occurs only when people are exposed to chronic infection—that is, multiple death-defying encounters with
P. falciparum
. It is as fleeting as a suntan. After all, malaria parasites reproduce new generations at a rate two hundred times greater than we do. A few months’ respite from the fiery glare of
P. falciparum
, and whatever immunity to the local parasite had been arduously acquired starts to fade away, canceled out by a new generation of the parasite. 53
    As a result, every year, many hundreds of thousands of people must face an invasion by falciparum malaria utterly defenseless. Throughhappenstance or lack of time, they have not built up any acquired immunity.
P. falciparum
destroys nearly one million of them every year. First and foremost, it kills the babies.
    Blantyre’s Queen Elizabeth Hospital is a sprawling, dusty complex of squat brick buildings surrounded by loud, traffic-clogged roads. People mill across its