VIRUS HUNTERS
On December 9, 2004, primatologists working in the Dja Biosphere Reserve in
southern Cameroon collected specimens from a dead chimpanzee. The chimp was
sprawled out on the forest floor, eyes closed, but seemingly unmolested by a
human or other predator. The team was rightfully concerned.
Belgian scientist Isra Deblauwe and her Cameroonian colleagues had started
their long, tedious work some three years earlier. In the tradition of primatologists
like Jane Goodall, their goal was to study wild great apes, our closest living rela-
tives, to learn about them and ourselves.
And a few years later, they produced some interesting results. The team re-
ported that, like other chimpanzee populations, the chimpanzees in the Dja used
tools. In particular, they modified sticks to extract honey from underground bee
nests. Chimpanzees, like all apes, including ourselves, love honey, and the infor-
mation from the Dja team would add to the understanding of how different chim-
panzee cultures use tools in different ways.
But on that rainy December day in 2004, honey was the last thing on the scien-
tists’ minds. Four days after taking samples from the first dead chimpanzee, they
took samples from another. Then on December 19 they took samples from a dead
gorilla. This was worrying. Since the primatologists only followed a fraction of the
population of apes in the Dja, what they’d seen was likely to be just the beginning.
Many other unidentified apes might be dead, valuable wild kin whom the team had
spent years working to understand. The consequences for conservation and re-
search could be considerable.
But the threat to wild apes, while significant, was not the only problem. The re-
searchers knew that the Ebola virus had wiped out large numbers of apes in
Gabon, only a few hundred kilometers to the south. Ebola not only kills chim-
panzees but from time to time has also jumped to humans causing dramatic and
potentially epidemic-inducing cases. They also knew that one of their primatologist
colleagues had acquired Ebola in the Ivory Coast when investigating deaths just
like these. Whatever caused these ape deaths was not to be taken lightly.
Fortunately, they had responded according to a plan. First and foremost, the
primatologists knew that they should not directly touch the carcasses. Months
earlier, when the first dead animals had been seen, they had sent a message to col-
leagues in Yaoundé, Cameroon’s capital. The message in turn was transmitted to
Mat LeBreton, the dedicated and skilled biologist who leads our ecology team and
has pioneered a number of new techniques in viral ecology. Based in Yaoundé,
LeBreton helped support an international team, including relevant ministries and
laboratories in central Africa and Germany on the outbreak investigation that would
follow.
The investigating team rapidly put together and deployed a mission to the Dja, a
stunningly beautiful and unique rain forest habitat located along one of the major
tributaries of the massive Congo River. There they worked with the primatologists
to collect the specimens. They managed to obtain specimens from the skull and
shoulder of the first chimpanzee. They also collected a specimen from the leg of
the second chimpanzee, the jaw of the gorilla, and some muscle from a fourth vic-
tim— chimpanzee—who died in early January 2005.
The safely preserved specimens then made the trip to expert laboratories. They
went to the high containment laboratory of Eric Leroy, the virologist whom we
worked with to discover the new strain of the Ebola virus discussed in chapter 5.
The specimens also went to our collaborator Fabian Leendertz, a veterinarian and
microbiologist working at the Robert Koch Institute in Germany who has perfected
the study of ape microbes during many years spent shuttling between field sites in
Africa and his lab in Berlin.
The results were surprising. While we all had come to assume that the same
wave of Ebola knocking down ape populations south of the border in Gabon had
killed the animals in the Dja, the specimens all came back negative for the Ebola
virus. They were, however, all positive for another deadly agent—anthrax.
In 2004 Leendertz and his colleagues had reported a similar die-off of chim-
panzees in the Taï forest of the Ivory Coast due to anthrax. So while the gorilla
death in the Dja was the first of its kind, anthrax was already known to be a killer of
forest apes. Strange perhaps but not unprecedented. How exactly a bacteria nor-
mally found in grasslands ruminants got to the apes in the Dja and Taï forests is
still a mystery. There were some theories. Anthrax spores remain viable for long
periods of time, even up to a hundred years. The spores can contaminate water
supplies, so the apes may have picked it up from lakes or creeks. They may also
have become infected while hunting or scavenging on ruminants, such as forest
antelopes, that had themselves been infected. Or perhaps, at least in the Taï forest
outbreak, neighboring farms had seeded the outbreak when the apes had foraged
for food in cropland contaminated by anthrax from cattle.
Whatever the route of infection, the findings from the Dja and from the earlier
animal epidemic in the Ivory Coast showed that the declining populations of
African apes had more than hunting and habitat loss to blame. Viruses like Ebola
have swept through large swaths of the remaining habitats of wild apes, and now
anthrax must also be considered a threat to these valuable wild animals. From a
personal perspective, having worked with wild chimpanzees and helped habituate
populations of gorillas in Uganda, I feel that the mounting threats to our closest
living relatives is a tragic loss to the heritage of our particular form of life.
From the perspective of my work tracking and preventing pandemics, the
deaths pointed out another glaring weakness in the way that we catch these
epidemics. The discovery of anthrax in the Dja forest did not represent a success in
pandemic prevention. It was rather the epidemiological equivalent of dumb luck.
Only a trivial fraction of the global ape populations are under the watchful eye of
woefully underfunded primatologists. If we’re relying on these scientists to regu-
larly capture the animal epidemics that could signal future human plagues, then
we’re destined to fail. To truly catch epidemics early, we’ll need much more.
How can we hunt down deadly viruses and control them? A few primatologists
finding dead animals is not a surveillance system. But what is the right way to
catch new epidemics and stop them before they spread? This section will explore
just that: the contemporary science of pandemic prevention. It will discuss the
ways that my team and other colleagues and collaborators are working to create
systems that will be able to catch and stop new epidemics before you (or CNN)
even know about them. Preventing pandemics is a bold idea, yet no bolder than
when cardiologists in the 1960s began to think that they could prevent heart at-
tacks, a medical advance that was radical at the time but is now largely taken for
granted.
My own thinking on this dates to the late 1990s when I joined Don Burke at
Johns Hopkins and agreed to establish a field site aimed at monitoring humans
and animals for new viruses in central Africa. It was an exciting time, when the idea
that simply responding to pandemics would no longer be sufficient was truly in the
air. I remember spending many afternoons in Don’s office alternating between ur-
gent scribbling on the whiteboard and thinking out loud about what would be
needed to accomplish the task.
Among the ideas that we generated during that time, one lasting concept partic-
ularly stands out: viral chatter. When he coined the term, Don did so as a direct
parallel to intelligence chatter. One way of thinking about this is to ask the question:
how do security services prevent terror events?
Intelligence services use a range of techniques to monitor for potentially threat-
ening events, but among their most valuable tools is the monitoring of chatter.
Intelligence agencies scanning e-mails, phone calls, and online chat rooms can fol-
low the frequency that certain signals occur. If a journalist were to fire off an e-mail
that included the words al-Quaeda and bomb for example, it would be picked up by
an automated system that filters for suspicious key words. Having said that, it
would not likely make it to the desk of an analyst, since the systems also register e-
mail accounts and IP addresses and would hopefully flag the chatter with journalist.
During testimony on the September 2001 attacks on the United States, the for-
mer CIA director George Tenet said that the “system was blinking red” in the
months leading up to 9/11. Similarly, although it was an accidental event, the day
that the Chernobyl reactor melted down in 1986 there was a significant spike in
message traffic in the former Soviet Union. Knowing what sorts of key words to
look for and who the usual suspects are, as well as understanding how they
communicate with each other can provide valuable intelligence to help predict rare
but important events.
As Don and I considered it, we asked ourselves what a global system to monitor
the viral equivalent of such chatter would look like. How could we monitor the
many thousands of interactions that occur between humans and animals in order
to detect the chatter events—in our case the jumping of novel viruses to hu-
mans—that would signal a looming plague?
Clearly, a system that depended on communities like the primatologists, whose
primary focus was studying animal behavior and ecology, would not be sufficient.
An ideal system would monitor global viral diversity in humans and animal popula-
tions and detect when agents jumped from animals to humans. While theoretically
possible, such a system defied resources and technology at the time.
As we’ll discuss in greater detail in chapter 10, the current laboratory methods
for accurate and comprehensive surveys of the diversity of viruses in people and
animals, while improving all the time, are not yet at the point of being deployed
globally. Also, the simple logistics of monitoring everyone would be impossible.
To begin, we’d need a much more focused system—a system focused on a small
set of sentinels, key populations that would allow us to monitor viral chatter with
the resources we currently have.
I remember vividly the first time I thought about the role of hunting in the trans-
mission of infectious agents. While a graduate student at Harvard, I spent my first
two years focused on the study of wild ape populations. Among the pleasures of
being a graduate student in the Department of Biological Anthropology was being
able to interact with one of the leading professors, Irv DeVore. Irv, a leading teach-
er and thinker in primatology and human evolution, has a striking head of white
hair and a Vandyke beard to match. The son of a Texan Baptist minister, he taught
human evolution with the fervor of an evangelist and is beloved among the scores
of prominent scientists who benefitted from his tutelage.
From 1993 through 1995 I worked for Irv as a teaching fellow for the class he co-
taught at the time with the Harvard psychologist Marc Hauser. The course, Human
Behavioral Biology, was referred to as “Sex” by the Harvard undergraduates be-
cause of the focus on human reproduction. During those years, I had the oppor-
tunity to meet with Irv in his office on the top floor of the Peabody Museum and on
occasion at the wonderful evolution-soaked beer hours that proliferated at faculty
homes.
On one particularly memorable afternoon, I remember speaking to Irv in his
wood-paneled office in the Peabody. During our freewheeling conversation, the
topic reverted to my growing obsession at the time—microbes. It was then that Irv
told me a story that would help put me on the research track I’ve taken for the last
fifteen years.
During one of his summers spent on Martha’s Vineyard, Irv had come across a
dead rabbit while driving home. Assuming it was a healthy animal that had been
killed by a car and being a lifelong hunter who had worked with indigenous hunters
throughout the world, Irv did what seemed natural for him. He picked up the rabbit
and brought it home, where he subsequently dressed and cooked it for supper.
Within a few days Irv was very ill. He experienced fever, diminished appetite,
and severe exhaustion. His lymph nodes enlarged. Fortunately, he went to an
emergency room immediately, because as it turned out he’d acquired tularemia, a
potentially fatal bacteria that often infects wild rabbits and other rodents. Death oc-
curs in less than 1 percent of people with prompt treatment, but had he not been
treated quickly, he may very well have died a painful death from multiple organ fail-
ure.
Irv likely acquired tularemia when skinning the infected rabbit. A common route
of entry for this bug occurs during butchering, when the bacteria can be inhaled
into the lungs. By the time Irv finished his story, my mind was racing with the
possibilities. One of Irv’s earlier works was a book called Man the Hunter, and he’d
spent many years living with hunter-gatherer populations in Africa, populations
that don’t practice farming and live exclusively on wild foods. Our conversation
veered to the idea of working with these populations, who no doubt had extraor-
dinarily high rates of exposure to the microbes in the animals around them.
In 1998, a few years after my conversation with Irv, I wrote about the role of hunt-
ing in disease transmission. In the article, I proposed that hunters could act as
sentinels—and if we studied them over time we could get a sense of what, how,
and when microbes were jumping into humans. During my conversations with
Don Burke a few years later, this became a common point of discussion for us as
we explored the concept of viral chatter. How might hunters lead us to the critical
microbes making that fateful jump into the human species?
When Don recruited me to join his growing program at Johns Hopkins, he had
already established a close collaboration with a Cameroonian scientist examining
retroviruses, like HIV, in the region of central Africa where they originally emerged.
I would spend many years working with Don and the Cameroonian colleague,
Colonel Mpoudi Ngole. During those years, we would put the foundation in place
for the first real system attempting to catch novel pandemics before they emerge.
One of the first people I met when I arrived in central Africa was the aforemen-
tioned Colonel Mpoudi (pronounced m-POODY), a large, imposing, mustachioed
man who so consistently wore a uniform that I wondered at times if he slept in it.
The Colonel, as I refer to him to this day, is a quiet but incredibly productive physi-
cian and scientist. He is known by many of the people in Cameroon as Colonel
SIDA (SIDA is the French acronym for AIDS) for his years of relentless work to
stem the tide of the AIDS pandemic in central Africa. The Colonel has a subtle yet
commanding presence, and he’s used to getting his way. During my first years in
Cameroon, we did battle from time to time, fighting over the best way to use scarce
resources. Yet I always respected him as an effective and caring leader who knew
how to negotiate better than anyone I’ve ever met, and even more importantly knew
how to get things done. Over time, he came to be an important mentor and dear
friend.
Among the subjects that Don and the Colonel had thought carefully about was
bushmeat, and it would be a central subject for the work we’d do in central Africa.
Bushmeat is another word for wild game, although historically the term tends to
refer to wild game in tropical locations. In reality, when my friends hunt and eat
venison in their yearly New England ritual, they’re eating bushmeat. And when I
visit my favorite seafood place in San Francisco—Swan Oyster Bar—the living sea
urchin they carve open and serve me in the shell is also bushmeat. Yet as we
learned in chapter 2, from the perspective of microbes not all bushmeat is created
equal.
When we started our work in Cameroon, the overriding objective was to under-
stand why HIV in central Africa was so diverse compared to the fatal but genetically
bland and homogenous cosmopolitan versions of the virus that hit most of the
world. The idea was to sample HIV from people throughout rural regions and
hopefully explain why so many different genetic variants of the virus existed in this
part of the world. All of the evidence pointed toward this region as the place where
HIV began, but why did it remain so diverse twenty years after the pandemic had
exploded?
To answer the question, we teamed up with some of Don’s former colleagues at
WRAIR (Walter Reed Army Institute of Research), where he had spent most of his
career. I remember first meeting the dynamic duo—Jean Carr and Francine Mc-
Cutchan—at their unremarkable office space in unremarkable Rockville, Maryland.
But there was nothing at all bland about the work they’d done.
Over the five years before I met them, the pair had revolutionized the study of
HIV by creating methods to sequence entire HIV genomes and systematically study
where their various genetic bits and pieces had come from. Prior to their work,
people had largely stitched together smaller pieces of genetic information to get a
picture of the sequence of the entire virus. Carr and McCutchan had come up with
a way to pull the entire ten thousand bits up in one fell swoop. This permitted them
to dive into the history of the different genes that made up the viruses.
Since HIV recombines, or has the capacity to mix and match genes among dif-
ferent strains, they needed to form a new set of analytical tools to understand
which bits fit together and from where each bit had descended. They were prac-
ticing virus genealogy. But instead of piecing together the ancestry of a Scandi-
navian monarch, they were determining the parental strains of particular HIV virus-
es and mapping them globally to try and reconstruct the course of the pandemic—
plotting out a map of how HIV had spread and mixed.
Along with a dedicated team of local scientists, the Colonel and I would work
over the next few years to try to sort out the causes for the intense genetic diversity
of HIV in central Africa. Basically, we wanted a snapshot of what HIV looked like
before it went global. We started by setting up shop in rural villages throughout
Cameroon. The work in the villages was coordinated by Ubald Tamoufe, a soft-
spoken and highly meticulous engineer turned biomedical scientist, who still co-
ordinates our joint work in central Africa. We didn’t pick just any rural villages. In
order to avoid capturing the relatively boring garden-variety strains of HIV that now
spread throughout the globe and even in regions like Cameroon where the pan-
demic began, we picked isolated villages found where the roads end.
To say these places were challenging to get to only hints at the complex logistics
required to obtain the high-quality specimens Carr and McCutchan needed. These
were some of the most remote regions of central Africa. Among their incredible
stories comes one from a beloved project driver, Ndongo, who like the Colonel,
was largely referred to by his rank, sergent-chef, rather than his proper name. Ser-
gent-Chef once had to abandon his car on one side of a river, then crossed it by
small canoe to help our team get specimens from the small village of Adjala in the
far southeast of the country.
Obtaining the specimens from these incredibly remote locations held out par-
ticular challenges and frustrations but also wonderful experiences. During one
particularly memorable visit to a rural village, this one in DRC, I spent the day with
hunters in the forest. Upon my return, I learned that a baby boy had just been born
to a woman in the village and that they wanted to honor me by giving the child my
name. Since one of the villagers had heard me referred to as Docteur Natan
(French for “Dr. Nathan,” as I’m sometimes called in that part of the world), that
was the name they chose for the boy. Not “Nathan” but “Doctor Nathan.” The ex-
pert research logistician, Jeremy Alberga, who has kept our administrative, logis-
tical, and financial operations organized over the years, joked that the name would
decrease the need for burdensome higher education. The boy was already a doctor.
But what exactly were the specimens we were collecting? To start with, we need-
ed blood. From the people who enrolled in our studies, we collected two tubes of
blood using high tech tubes that would allow us to easily separate the different
parts of blood when we got back to the laboratory in Yaoundé. As for the animals,
at least to start with, we worked using a simple but innovative approach, a method
developed by Mat LeBreton.
When I originally met Mat in Yaoundé, he was just completing a monumental
survey of snakes in Cameroon. Interestingly, he’d done the majority of his sam-
pling by leaving pots of formalin preservative in villages across Cameroon. Since
humans throughout the world kill snakes when they find them, he simply asked
them to put the dead snakes in the formalin pots, which he’d collect from time to
time to study their distribution and diversity. As we talked, we realized that a sim-
ilar approach could be used to easily collect thousands of specimens from ani-
mals. We could adapt the filter-paper techniques I’d learned from Janet and Bal
Singh in Malaysia years ago and simply pass out the baseball-card-sized sampling
papers to hunters and let them collect specimens whenever they came into contact
with blood. The technique proved incredibly successful, and we now have among
the most comprehensive wild animal blood collections in the world.
In addition to the challenges of simply getting to tough places to collect spec-
imens, we had the difficulty of communicating our intentions to potential partic-
ipants in our studies. Gossip and rumors abound in these small villages, and the
villager’s range of speculations about nefarious purposes for the blood we needed
from them was broad. Fortunately, among the excellent staff were some of the
most talented communicators I’ve had the good fortune to work with.
Particularly notable was Paul Delon Menoutou, who had spent years as the chief
health correspondent for Cameroonian radio and television, joining us upon his re-
tirement. In many of the rural villages where we worked, people had never had ac-
cess to television and didn’t recognize his face, but when he began to speak, they
instantly knew his voice. As a trusted and amazingly talented communicator on
health issues, he helped us to ease our way into these communities, which could
otherwise resist answering the scientific questions we asked. He also helped con-
vey critical health messages that were a fundamental part of our mission.
Over the first few years in Cameroon, we managed to build a functional laboratory
in an amazing century-old building that hailed from the German colonial period in
the capital of Yaoundé. We also established connections to seventeen rural villages
in fascinating, biologically diverse parts of the country. The high-quality frozen
specimens we obtained held clues to the problems of explaining HIV diversity and,
as we’d find, much more.
By the time they got into the Rockville laboratories, the specimens had moved
thousands of miles by road and air yet remained frozen and viable for testing. I
spent some time working in the lab myself, anxious to see exactly what was in the
specimens. However, much of the heavy lifting of characterizing the viruses in the
specimens was left to McCutchan and Carr and their capable lab teams.
In the end, they found remarkable diversity in these HIV specimens. Twelve of
the villages we worked in had completely unique forms of HIV—viruses that were
patched together of different sorts of HIV variants, ones that had never been seen
together before. In nine of the villages, there were two or more of these unique
forms of HIV. Our conclusion was that these locations likely showed what HIV
looked like prior to its global spread. Essentially, following the entry of the virus
from chimpanzees in the early twentieth century, it likely maintained itself in small
villages like the ones we’d studied. Over time, as the virus changed, the newly di-
verged forms came into contact with each other, shuffling their genetic information
and producing an incredible assortment of genetic novelties. Only some of these
strains would win the microbial lottery and spread. The rest would remain inter-
esting viruses near the place where their ancestor viruses continued to live in wild
chimpanzees, staying put but almost certainly causing disease like their more pro-
lific kin.
While in these rural villages, we did more than just collect specimens to answer
our questions about HIV diversity. We also looked into the ways that people inter-
acted with wildlife, a study coordinated at the time by Adria Tassy Prosser, an an-
thropologist and epidemiologist now based at the Centers for Disease Control in
Atlanta. We learned that people in these rural villages had an incredible and inti-
mate level of contact with wild animals. The process of butchering involved direct
contact with virtually all of the blood and body fluids that viruses call home. As we
provide basic food to needy families. It is subsistence, not entertainment. Hunting
is hard work. It requires tremendous energy for a fairly modest outcome in calories.
While many of the hunters we work with are excellent at hunting and some even
enjoy it, most would likely choose a cheap and nutritious form of protein that
didn’t involve hours tracking through incredibly hard-to-negotiate landscapes—
fish, for example. I remember my encounter with a man who was headed to his vil-
lage, carrying a monkey he’d hunted on his back. One of my first thoughts when
looking at the bloody and battered animal was how unfortunate it was to lose such
a beautiful and important part of our planet’s wild heritage. But I also saw that the
man was wearing flip-flops and ragged clothing and was sweaty and dirty from a
whole day in the forest. He certainly was doing this for his livelihood and not for
sport! Subsistence-level hunters are not the enemies and, as we’ll explore further in
chapter 12, the solution is to work with them rather than against them.
As we pushed forward with our work to characterize the diversity of HIV among
these rural hunting communities, we also began what would become a main focus
of my work over the past ten years—to discover completely novel viruses jumping
into these highly exposed peoples. To do so, we approached one of the world’s top
laboratory teams for discovering novel retroviruses, the broader family of viruses
that includes HIV—the CDC’s Retrovirology Branch.
The CDC team included Tom Folks and Walid Heneine, two of the world’s lead-
ers in retrovirology, but the person I’d spend most of my time working with was
Bill Switzer. Bill has a youthful appearance that belies his actual age and a mellow
demeanor that masks his relentless drive to chart the evolution of some of the
most interesting viruses of our time. Whether face-to-face or by phone, Bill and I
would spend the next ten years working together on an almost daily basis to assess
what viruses besides HIV had jumped into those hunting populations.
My first major discovery with Bill was of an ominously named virus, the simian
foamy virus (SFV). SFV received its name because of the way it kills cells. When
you look at a culture infected with the virus, the cells die and bubble up, leading to
a foamy appearance under a microscope. It’s a virus that infects virtually all non-
human primates. And since each primate has its own particular version of the
virus, it provides a great model for comparison. By sequencing the viruses, if we
were then to find one in humans we’d know exactly what animal it had come from.
Interestingly, humans have no indigenous foamy virus. Bill and his colleagues
showed some years ago that foamy virus has the unusual feature among viruses of
cospeciation. In other words, the common ancestor of all living primates some
seventy million years ago had a foamy virus, and as the various branches of the pri-
mate tree speciated over time, the virus passed along. The amazing result is that
the evolutionary tree of foamy viruses and the evolutionary tree of primates are
virtually identical. SFV may very well have been one of the viruses we lost during
the pathogen bottleneck discussed in chapter 3.
When Bill and I and our colleagues started the work with primate foamy viruses
we already knew that they could theoretically infect humans, as a few lab workers
had previously acquired the virus. But we had no idea if this occurred under natural
settings. We were surprised and quite excited to find that it did. I remember well
the exact day it became clear. We were working together in Bill’s lab, and I went
downstairs to get the images of a lab test called the Western blot, which shows
whether or not individuals have produced antibodies against, in this case, the simi-
an foamy virus. Bill came down that day to help me interpret the images. As soon
as we saw the results, it was obvious that some of our study participants had been
infected. I remember Bill and I looking at each other with equal parts shock and ex-
citement. In a tangible way the work over the past years changed dramatically at
that moment. To this day I have a framed copy of the Western blot on my wall.
On the one hand, there was relief—the research had succeeded. But there was
also a sense of foreboding for us—retroviruses, viruses from the class that had
produced HIV, were crossing into humans. And if we were seeing it within the first
few hundred hunters we’d studied, it was by no means rare.
Over the coming months we saw that in fact a number of the people in our
study who had reported hunting and butchering nonhuman primates had been ex-
posed to SFV. More amazingly, some of the exposures had gone on to become
long-lasting infections. After finding evidence that these individuals produced anti-
bodies to the virus, we tried to obtain actual SFV genetic sequence, and what we
saw surprised us. We found multiple people who were infected with strains of SFV
from primates, ranging from the DeBrazza’s guenon, a small leaf-eating monkey, to
the massive lowland gorilla. To our great satisfaction, we found that the results of
our behavioral surveys matched. The gorilla SFV, for example, came from a man
who had reported hunting and butchering gorilla meat. While many of the people
in our survey had exposure to primates, few participated in the dangerous and
highly specialized hunting of gorillas. The link was a smoking gun—the gorilla
hunter had acquired the virus while hunting or butchering his prey.
The finding provided both a sense of adulation and fear. Most virologists would
be lying if they said they didn’t enjoy finding something completely new. It had
taken us years of hard work to line up the funding, find the local collaborating
scientists who knew how to accomplish the work, set up a lab in central Africa,
establish village outreach, collect specimens, store and ship them through the
complexities of international agreements, and conduct the complicated laboratory
work necessary to find an actual virus. The results showed that our system worked
and that we were right in guessing that high levels of exposure to animals would
lead to infection with novel viruses. Yet, the first evidence that new retroviruses
were moving into humans also suggested that people’s faith in the existing public
health structures—that they would inform us when novel viruses were moving into
humans—was misguided. We were only beginning to see just how misguided it
was.
In the following year, we went on to study yet another group of retroviruses, the
T-lymphotropic viruses (TLVs). SFV was a virus with no real human precedents.
Before our work, only a handful of laboratory workers had been infected, so deter-
mining how much the virus was likely to spread and cause disease—and its poten-
tial to become a pandemic—was unclear. Not so for the TLVs. It’s long been
known that humans around the world are infected with two different varieties of
TLV—HTLV-1 and HTLV-2; in fact, some twenty million people have these viruses.
While some individuals can be infected without disease, many get sick from ill-
nesses ranging from leukemia to paralysis. These viruses have pandemic potential.
Clearly, if completely novel TLVs were moving from animals to humans, public
health officials should know about it. Our results from SFV suggested this was a
real possibility.
Going into the study, Bill and I knew that each of the two varieties of human
TLV came from primates—just as HIV had. We also knew that another group of
TLVs existed in primates that hadn’t yet been found in humans—the Simian T-
lymphotropic Virus 3, known as STLV-3—so we began there. We screened the sam-
ples carefully, and as predicted, we found it—a virus infecting human hunters that
was clearly unlike HTLV-1 and HTLV-2 and fell squarely with the viruses in the
STLV-3 group. This was an important scientific finding for us. STLV-3 had the
potential to cross into humans and was on the move. Even more surprising was an
entirely new human TLV found in a single individual from eastern Cameroon—a
virus we called HTLV-4.
The combination of finding a number of new SFVs in people exposed to pri-
mate bushmeat in central Africa and two entirely novel TLVs in the same popu-
lation changed the way that we thought about our work. While it was theoretically
clear that people exposed to a wide range of wildlife would acquire microbes from
these animals, we didn’t know at the start whether monitoring those populations
was practical or what such a system would look like. As we began the long and
plodding work to determine the extent to which the new SFVs and TLVs were
spreading and causing disease (work that continues to this day), our thinking
opened up. We began to seriously consider that monitoring people highly exposed
to wildlife could be a globally deployed system to capture viral chatter.
In 2005 I took a long shot. I applied to an unusual program sponsored by the Na-
tional Institutes of Health (NIH), the largest government funder of biomedical re-
search in the world. The NIH had supported my work in the past, but the world-
class institution didn’t perfectly match the work I hoped to do in the future. While
the NIH has a broad ranging program, it does not distribute its resources evenly.
The NIH specializes in funding laboratory research rather than field research. It fo-
cuses its energy largely on research in more reductionist cell biology—work that
focuses on very clear hypotheses that provide very clear yes or no answers. A pro-
gram to spearhead a brand-new global monitoring effort to chart viral chatter and
control pandemics was not something that would normally be supported. Yet in
2004 the NIH began a completely new program—the NIH Director’s Pioneer
Award Program—aimed at sponsoring innovative research not normally supported
by the NIH mission. The program gave grantees $2.5 million and five years to do
largely whatever they felt was necessary to advance their scientific objectives. In the
fall of 2005 I was among the fortunate individuals to get the award.
At this point, the pieces were beginning to fall into place. Certainly $2.5 million
was nowhere near what would be needed to roll out a global monitoring system,
but it was a good start. It allowed me to begin truly thinking about which key viral
hotspots around the world needed the most urgent monitoring. Some key regions
came to mind right away. The work with Jared Diamond and Claire Panosian had
shown that Africa and Asia provided the lion’s share of our major infectious dis-
eases. Those would be the places to start.
In the coming years, along with my team and a stunning range of local collab-
orators, I would take the model we’d developed in Cameroon and begin to deploy it
in a number of other countries in central Africa. With the help of dedicated field
scientists like Corina Monagin, who has become expert at making field sites in
sensitive and difficult areas function, I’d renew collaborations from my years in
Malaysia and begin to work with new sets of colleagues to establish programs in
China and Southeast Asia. We’d set up the beginnings of a system to capture glob-
al viral chatter. Along with a growing number of colleagues worldwide, we would
push ourselves to ask how we could best find new viruses. How could we capture
a much higher percentage of the new viruses killing humans and infecting animals?
In the coming chapters, we’ll explore the results of this work. I’ll also discuss
some of the cutting-edge tools employed to improve our ability to detect pan-
demics before they spread. While the threats associated with pandemics are large
and growing, so too are the approaches and technologies to address them.
