The Viral Storm (8 page)

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Determining historic population sizes, particularly prior to periods in which we have written records, is fraught with difficulty. But studies suggest that our ancestors’ population densities were sometimes very low, with lower numbers than those of current gorilla and chimpanzee populations, and at least once teetered on the brink of extinction. Our ancestors would have been an endangered species. We believe this to be the case because our genes maintain some of these records, and by comparing the genetic information among contemporary human populations with that of our close ape relatives, we can tease out inklings of relevant information.

The information revealed is striking. Analyses of the human mitochondrial genome, a region of genetic information that passes only from mother to daughter, as well as studies of mobile genetic elements that accumulate in regions of the genome in a clocklike way provide clues to our historic population size and suggest it was much smaller than we might expect.

Our preagricultural ancestors likely lived in small groups, which is not necessarily surprising. Most of our evolutionary history as primates was spent in forested environments. And while exact timelines for the main events remain unknown, moving from forested environments to savanna habitats, shifting from largely fixed territories to a more nomadic lifestyle, and adapting to the various new conditions imposed by these changes must have been traumatic. An apt comparison might be the idea of contemporary humans living on Mars. The generations of our ancestral populations that confronted the savanna frontier probably did so at some cost. But our interest in small population sizes here is less about the consequences for humans and more about the consequences for microbes.

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Low population densities, such as those exhibited by our ancestors, have a marked impact on the transmission of infectious agents. Infections need to spread. If population sizes are low, it is much harder for this to happen. The scientific term for substantially reduced population sizes is
population bottlenecks
, and when population bottlenecks occur, species should be expected to lose their microbial diversity.

Microbes can be largely divided into two different groups, acute and chronic, and each group is impaired in small host populations. In the case of acute agents (like measles, poliovirus, and smallpox) infections are brief and lead either to death or immunity from future infections: they kill you or make you stronger. Acute microbes require relatively large populations; otherwise, they will simply burn through the susceptible individuals, leaving only the immune or the dead. In either case, they go extinct. If there’s no one left to infect, that’s the end of the line for a microbe.

Chronic agents (like HIV and hepatitis C virus), unlike acute agents, do not lead to long-lasting immunity in their hosts. They hang on to their hosts, at times holding on for a host’s entire lifetime. These agents have a better capacity than acute agents to survive in small populations. Yet during severe population bottlenecks, even chronic agents suffer from higher rates of extinction. Just like the probability that a particular gene will be lost during a population bottleneck (a phenomenon that results in inbreeding in small populations), the probability that a chronic agent will be lost should also be expected to increase when populations are small. If someone dies, and they are the last individual carrying the microbe, then the microbe dies.

The role of population bottlenecks in diminishing microbial repertoires, what I call
microbial cleansing
, likely had an effect when the population sizes of our ancient ancestors crashed, resulting in populations with a lower diversity of microbial agents. In some cases, microbial cleansing would have led to situations where agents present for millions of years in our ancestors disappeared. Agents that had accumulated following the advent of hunting and other agents that were simply part of our heritage just vanished. While we don’t normally think of microbes as a part of our family heritage, in many ways that’s exactly what happens—they pass down to us from our ancestors, but from time to time they die out. And while microbial cleansing sounds like a very good thing, it would prove to be a double-edged sword.

A population bottleneck: a diverse population (top) is greatly diminished by a near-extinction event (middle), resulting in a more homogenous population (bottom).
(
Dusty Deyo
)

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Sometime following the split between the chimpanzee/bonobo lineage and our own, another important change occurred in our ancestors that would have dramatic consequences for our microbial repertoires: they learned to cook. Not Michelin three-star cuisine, of course, but cooking nonetheless: using heat to prepare food. Exactly when our ancestors harnessed the power of fire remains a mystery. Presumably, fire first provided warmth and security from predators and competitors. Yet it appears to have quickly become a profound way of altering food. Richard Wrangham, my mentor from Harvard, discusses cooking and its consequences in depth in his well-researched book
Catching Fire: How Cooking Made Us Human
. Among other things, he analyzes in detail cooking’s origins.

When our ancestors began to cook extensively, in addition to the advantages that cooking offered them by making food more manageable and palatable, they also benefited from its remarkable ability to kill microbes. While some microbes can survive at incredible temperatures (such as the hot spring microbial hyperthermophiles that grow and reproduce at temperatures above the boiling point of water), the vast majority of microbes that make their living off of animals cannot survive the temperatures associated with cooking. As microbes are heated during cooking, their normally solid, densely packed proteins are made to unfold and open, allowing digestive enzymes quick and easy access to destroy any capacity to function. As with the population bottlenecks that our ancestors swung through, the cooking that became their standard way of life served to again diminish their uptake of new microbes, helping limit their microbial diversity.

The earliest solid evidence that humans controlled fire comes from archaeological finds in northern Israel where burned stone flakes dating back almost eight hundred thousand years were found near fire pits. This is almost certainly an underestimate. African sites dating to over a million years ago contain burned bones that could be the remains of cooking, yet the lack of archaeological evidence makes these finds more ambiguous. In Wrangham’s analysis, the evidence of cooking goes back much further. By examining the remains of our ancient ancestors, paleontologists have found physiological clues indicating that they consumed cooked food. For example
Homo erectus
, a human ancestor from 1.8 million years ago, had exactly the larger bodies and smaller digestive tracks and jaws to imply that they consumed higher-energy diets that were easy to chew and easy to digest—in other words, foods that had been cooked.

Whatever the exact date of our ancestors’ culinary dawn, it has certainly exploded since then. Cooked foods make up the vast majority of contemporary diets. In my work with hunters around the world, I’ve had a chance to sample from a vast range of these foods—from roasted porcupine and python in Cameroon to fried wood grubs in rural DRC. On one occasion, my “friendly” Kadazan collaborator in Borneo even gave me dog stew as a practical joke (I didn’t really see the humor). I’ve had a chance to sample food far beyond the beef, lamb, and chicken staples that I grew up eating in America. Yet no matter what I’ve eaten, or where I’ve eaten it, one thing can be certain: if the food has been cooked sufficiently, the likelihood that it will make me sick is small.

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The dual factors of diminished population sizes and cooking were not the only things that served to decrease the microbial repertoires of our early ancestors. The transition from rain forest habitat to a savanna habitat meant different vegetation and climate but also an entirely different set of animals to interact with and hunt. And different animals meant different microbes.

While we still understand very little about the ecological factors that lead to microbial diversity, there are some key factors that certainly play a role. We know, for example, that the biodiversity of animals, plants, and fungi supported by tropical rain forest systems is higher than any other ecosystem on land. When our ancestors left the rain forest, they entered into regions with diminished biodiversity. The diversity of microbes would almost certainly have been reduced, as would the diversity of the host animals that they infected. So the savanna grassland habitats likely housed fewer animals and a lower diversity of microbes capable of infecting them, which in turn contributed to lower microbial repertoires for our ancestors.

The kinds of animals living in the savanna also differed in critical ways from those in the forests, including a marked contrast in the diversity of apes and other primates. Simply put—primates love forests. The king of the jungle is a primate, not a lion. While some primates, like baboons and vervet monkeys, live very successfully in savanna habitats, forest regions trump savanna regions in terms of primate diversity. When we consider the microbes that could most easily infect our ancestors, the diversity of primates in any given habitat plays an important role. They are certainly not the only species that contribute to our microbial repertoires—in my own studies, I focus not only on primates but also on bats and rodents—but they do play an important role.

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Some years ago, I began considering what factors might improve or decrease the chances that a microbe would jump from one host to the next successfully enough to catch on and spread in the new host. It may seem that bats and snakes, for example, would provide similar sources for novel microbes. Yet there is a strong argument against this idea. Long evident to those doing work on microbes in laboratories is the fact that closely related animals have similar susceptibility to certain infectious agents. So a mammal, like a bat, would have many more microbes that could be successfully shared with a human than a snake. If not for the logistics and ethics, chimpanzees would make the ideal models for studying just about every human infectious disease. As our closest living relatives, they have nearly identical susceptibility to the microbes that infect us. Over time, less and less laboratory research on human microbes is conducted in chimpanzees, but this is largely because of the valid ethical concerns associated with conducting research on them and the difficulty of controlling these large and aggressive animals in captivity.

Closely related animal species will share similar immune systems, physiologies, cell types, and behaviors, making them vulnerable to the same groups of infectious agents. In fact, the taxonomic barriers that we place on species are constructs of our own scientific systems, not nature. Viruses don’t read field guides. If two different hosts share sufficiently similar bodies and immune systems, the bug will move between them irrespective of how a museum curator would separate them. I named this concept the academically accurate but unwieldy
taxonomic transmission rule
, and it holds up for chimpanzees and humans as it would for dogs and wolves.
1
The idea is that the more closely related any two species are, the higher the probability that a microbe can successfully jump between them.

Most of the major diseases of humans originated at some point in animals, something I analyzed in a paper for
Nature
, written with colleagues in 2007. We found that among those for which we can easily trace an animal origin, virtually all came from warm-blooded vertebrates, primarily from our own group, the mammals, which includes the primary subjects of my own research, the primates, bats, and rodents. In the case of primates, while they constitute only 0.5 percent of all vertebrate species, they seeded nearly 20 percent of major infectious diseases in humans. When we divided the number of animal species in each of the following groups by the number of major human diseases they contributed, we obtained a ratio that expresses the importance of each group for seeding human disease. The numbers are striking: 0.2 for apes, 0.017 for the other nonhuman primates, 0.003 for mammals other than primates, and a number approaching 0 for animals other than vertebrates. So as our early ancestors left the primate-packed rain forests and spent more time with lower overall primate biodiversity in savanna habitats, they moved into regions that likely had a lower diversity of 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.