Free The Viral Storm by Nathan Wolfe Page A

relevant microbes.
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    Multiple factors likely conspired to decrease the microbial repertoires of our early ancestors. As they spent more time in savanna habitats, our early ancestors interacted with fewer host species, and those hosts were on average more distantly related to them. The advent of cooking increased the safety of meat consumption and stopped many of the microbes that would have normally crossed over during the course of hunting, butchering, and ingesting raw meat. And the population bottlenecks that our ancestors went through further winnowed down the diversity of microbes that already infected them. All in all, the conditions associated with becoming human served to decrease the diversity of microbes present in our ancient relatives. Though many microbes undoubtedly remained in our early ancestors, there were likely far fewer than those that were retained in the separate lineages of our ape relatives.
    During the time that our own ancestors went through their microbial cleansing, their ape cousins continued to hunt and accumulate novel microbes. They also maintained microbes that would have been lost in our own lineage. From a human perspective, the ape lineages served as a repository for the agents we’d lose—a microbial Noah’s ark of sorts, preserving the bugs that would disappear from our own bloodlines. These great ape 2 repositories would collide with expanding human populations many centuries later, leading to the emergence of some of our most important human diseases.
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    Perhaps the single most devastating infectious disease that afflicts humans today is malaria. 3 Spread by mosquitoes, it is estimated to kill a staggering two million people each year. Malaria has had such a profound impact on humanity that our own genes maintain its legacy in the form of sickle cell disease. Sickle cell, a genetic disease, exists because its carriers are protected from malaria. Protection was so important that natural selection maintained it despite the debilitating disease that appears in approximately 25 percent of the offspring of couples that each carry the gene. People who are afflicted with sickle cell have their origins almost exclusively in one of the world’s most intensely malaria affected areas—west central Africa.
    My interest in malaria is both personal and professional. During my time working in malaria-infested areas of Southeast Asia and central Africa, I was infected by it on three separate occasions. On the last of those occasions, I almost died. The first two times I’d had malaria were both in regions where malaria was common. I’d exhibited all the typical symptoms—severe neck ache (similar to how you’d feel if you slept in a strained position) followed by intense fever and profuse sweating. On each of my first two bouts, I simply went to a local doctor and received a quick diagnosis and treatment. While the pain and illness were miserable, they both resolved reasonably quickly.
    I was in complete denial at the time I had my third round with this deadly disease. I wasn’t in the tropics; I was in Baltimore! I had returned from Cameroon to do research at Johns Hopkins University, and I had very different symptoms, led by intense abdominal pain. I must have also had fever since I remember complaining to friends who were putting me up in their local bed and breakfast that my room was too cold. These new symptoms and the fact that I’d left Africa many weeks earlier fed my denial that this could possibly be malaria. I finally realized I needed urgent care while sitting half delirious in a tub of scalding water and watching the overflow hit the floor of my friends’ bathroom. Although I recovered after a few days in the hospital, the illness brought home for me the huge impact that this disease has on the millions of people who are regularly sickened by it.
    My professional interest in malaria had started much earlier. As a doctoral student studying the