VIRAL RUSH
Imagine the following. In a large city, let’s say Manila, residents in a densely packed
residential district report foul odors to local environmental health offices. Some
hours later small pets begin to fall sick. Veterinarians confirm an uptick in the
number of sick animals in the neighborhood. Around twenty-four hours after the
first calls reporting the strange smell, local physicians note an increase in patients
reporting blisters and ulcers on their skin. A few individuals report nausea and
vomiting.
At around forty-eight hours the first patients hit the emergency rooms. They
have fever, headache, shortness of breath, and chest pain. Some of them appear on
the verge of going into shock. At the same time some of the individuals with nau-
sea are getting worse—they’re experiencing bloody diarrhea.
As the days go on the numbers increase. By the end of the first week, nearly ten
thousand individuals have been hospitalized. Over five thousand of these people
have died painful deaths. At the end they can barely breathe—their skin blue from
lack of oxygen. Eventually, septic shock and severe brain inflammation strike,
killing most of them. As the number of deaths increase, journalists flock to the
scene. Manila residents attempt a mass exit, and despite the best intentions of the
government, the city verges on the brink of widespread and crippling panic.
The case I’ve outlined is a hypothetical one. But just barely. In June 1993 the
Aum Shinrikyo cult aerosolized a liquid suspension of Bacillus anthracis from the
top of an eight-story building in the Kameido neighborhood in the eastern part of
Tokyo. They launched a bioterror assault on one of the largest and most densely
packed cities in the world.
The good news is that they failed. An analysis written in 2004 states that their
choice of a relatively benign anthrax strain, low concentrations of the bacterial
spores, an ineffective dispersal system, and a clogged spray device all served to
make the 1993 incident in Tokyo a flash in the pan. No humans got sick, although
some pets appear to have died as a result of the release.
If the Aum Shinrikyo cult had come across a more deadly version of anthrax and
used even slightly better dispersal systems, things could have turned out quite
similar to our hypothetical scenario above. We know that the apocalyptic cult had
looked for more than just anthrax. The group set up multiple laboratories and dab-
bled in cultivating many agents. They played with botulinum toxin, anthrax,
cholera, and Q fever. In 1993 they led a large group of doctors and nurses to the
Democratic Republic of Congo, ostensibly on a medical mission, but actually in an
attempt to bring back an isolate of the Ebola virus for use in their grim operations.
Even if they had succeeded in their anthrax release, the deaths and disruption
caused by Aum Shinrikyo would have been restricted to the individuals exposed to
the spores they released. Anthrax does not transmit from person to person.
Though deadly, it is not contagious. But anthrax is only one of many agents that
could be used by terrorist groups. Bioterror is among the most serious concerns
for security experts. It is an ideal tool for the weaker parties in so-called asymmet-
rical warfare, where enemies differ significantly in the resources and firepower they
can draw on for battle. Even a weak opponent, like a terrorist group, can wreak
havoc with the right combination of microbe and dispersal.
Microbes hold great potential for terror groups. They are much easier to gain
access to than chemical or nuclear weapons. And, critically, unlike either chemical
or nuclear weapons, they can spread on their own. They can go viral, which is
something that neither deadly sarin gas nor a dirty bomb could accomplish. Per-
haps the only comparable situation is the long-term horror of some nuclear fallout
expressing itself in generations of mutated offspring and high rates of cancer, as
seen in Hiroshima. But those insidious effects are environmental and thus rela-
tively slow. A fast-acting, fast-spreading viral weapon would have that impact over
days, not decades.
It would be a mistake to underestimate the risk for bioterror, and most who
study it contend that it is just a matter of time before it’s unleashed on a human
population.
The fact that deadly microbes can be made to proliferate under lab conditions,
whether in legitimate laboratories or fly-by-night terrorist workshops, adds another
dimension to global pandemic risk. While exceptionally unlikely, if terrorists ever
got their hands on one of the few remaining vials of smallpox, the results would be
devastating. While smallpox has been eradicated in nature, two sets of smallpox
stocks remain under lock and key—one at the U.S. Centers for Disease Control in
Atlanta and one in the State Research Center of Virology and Biotechnology (VEC-
TOR) in Koltsovo, Russia. Both facilities have high containment bio-safety level 4
facilities. There’s been debate about possibly destroying the remaining stocks in
these labs, but to date the decision has been deferred because of the potential ben-
efit of access to live virus for the production of vaccines and drugs.
Interestingly, in 2004 scabs from suspected smallpox were found in Santa Fe,
New Mexico, in an envelope labeled as containing scabs from vaccination. The
finding points to the possibility of other unknown lots of smallpox existing in a lab
freezer or somewhere else. If they were released purposely or accidentally, the
consequences would be devastating. Since smallpox has been eradicated, we no
longer inoculate against it. So, for smallpox, such a release would be a perfect
storm. For us, it would be catastrophe.
Another risk is what is increasingly referred to as “bioerror.” Unlike bioterror,
bioerror occurs when an agent is released accidentally but spreads widely. In 2009
Don Burke, the mentor of my postdoctoral fellowship, published a paper on the
emergence of influenza viruses. In it he analyzes a variety of influenza viruses that
have spread in humans. One of the more interesting examples is the November
1977 epidemic that affected the Soviet Union, Hong Kong, and northeastern China.
The virus involved was nearly identical to a virus from an outbreak over twenty
years before, and it hadn’t been seen since. Don and his colleagues echoed earlier
research on the virus noting that the most likely explanation was that a lab strain
had been accidently reintroduced into the lab workers and had spread from there.
Over the coming decades, as it becomes possible for the masses to have access
to detailed biological information and the techniques to make or grow simple mi-
crobes, the probability of bioterror and bioerror will only grow. While most people
normally think of biology as occurring primarily in secure labs, this may not always
be the way it works. In 2008 two teenage girls from New York City sent away spec-
imens of sushi to the Barcode of Life Database project, a fascinating early program
to simplify and standardize genetic testing. They wanted to determine if the high-
priced fish that they were buying was what it was sold as. They found that often it
wasn’t. But they also found a way to get genetic information that until then was
only available to scientists.
But the student sushi study was about more than discovering that some of the
sushi vendors in New York City rip off their clients. It was one of the first notable
examples of nonscientists “reading” genetic information. Early in the information
technology revolution, only computer programmers could read and write code, like
HTML. Then nonprogrammers began to read code, then write code, and now we all
regularly read and write code on blogs, wikis, and games. As with any system of
sharing information, what starts as something highly specialized often becomes
universal. In the not-too-distant future, the small group of people conducting do-it-
yourself biology may become the norm. In that world the need for monitoring to
control bioerror will be more than just theoretical. In a famous prediction made by
Sir Martin Rees, the former president of the Royal Society of London warned, “… by
the year 2020 an instance of bioerror or bioterror will have killed a million people.”
The chemistry to create a pipe bomb or a meth lab becomes the biology to create a
viral bomb.
In this chapter we will explore the next big killers—the microbial threats that keep
me awake at night. Certainly, bioerror and bioterror are among them. The frequency
of both of these threats will rise in the coming years, but at least for the moment,
the greatest risks we face are still those that exist in nature.
In some biological arenas, the age of discovery is over. We know the rate at
which we’ll discover new species of primates, for example, will be very low indeed.
For viruses, that’s not the case. My collaborator Mark Woolhouse, one of the early
leaders in the field of emerging infectious diseases, has put together real numbers
on this. He and his colleagues have plotted the rate of discovery of new viruses
since 1901. Their analysis suggests we’re nowhere near the end of viral discovery;
we’ll find on average one or two viruses per year over the next ten years, and that’s
likely a conservative estimate.
One of the reasons contemporary scientists are finding new viruses is that we’re
looking. Studies like the ones conducted by my research group, which we’ll dis-
cuss in the coming chapters, actively seek to find unknown viruses in humans and
new viruses lurking in animals that might be the next to jump. Genetic techniques
for uncovering the unknown microbial world are also advancing, which makes find-
ing these new agents easier and faster than ever. But intensive research and height-
ened attention are not the only reasons we’re seeing new things.
The combination of factors we’ve discussed in the previous chapters has cre-
ated the perfect conditions for maintaining new agents in the human species. We
live in a massively interconnected world. Links made by transport networks and
medical technologies radically increase the probability that an animal virus that en-
ters into us—no matter where—will be able to gain a foothold and spread. This
means that while some of the new things we’re finding might have crossed over in
the past, they haven’t persisted. From our perspective, they’re new.
On February 21, 2003, a man at the Metropole Hotel in Hong Kong was sick—very
sick. He had come from the nearby Guangdong province and had arrived at the up-
scale hotel, which has a fitness center, restaurants, a bar, and a swimming pool.
He stayed just one night in the now infamous room 911. And he would become
among the most famous “super-spreaders” of modern history.
A super-spreader is a person (or animal) who plays an outsized role in the spread
of an infectious disease. The resident of room 911 at the Metropole had severe
acute respiratory syndrome, or SARS, and his virus spread to at least sixteen other
individuals. They in turn spread the virus to hundreds of other individuals as they
dispersed to the far points of the globe—Europe, Asia, North America. Even three
months later, investigators were able to pull genetic information of the virus from
the carpet near room 911, information that likely got there from his coughing,
sneezing, or vomiting.
We do not know exactly how the resident of room 911 became infected with the
SARS virus. It may have been through contact with an infected animal. We now
know that SARS ultimately originated in bats. Because people in the Guangdong
province commonly eat wild animals and purchase them in live animal markets, or
wet markets, the resident of room 911 may have had contact with an infected bat
purchased in one such market. Alternatively, he may have acquired the virus from a
civet, a small carnivore and a delicacy in that region of China. By that time, civets
had acquired the SARS virus from bats. Or he may have been infected from a per-
son who had acquired the animal virus. Perhaps most likely the virus had spread
undetected for some time before he got it himself.
However the Metropole guest acquired the virus, his illness appears to have
sparked the SARS pandemic that would follow, a pandemic that would go on to in-
fect thousands of people in at least thirty-two countries on every inhabited conti-
nent and have an economic impact measured in billions of dollars. The SARS pan-
demic provides a perfect example of how our modern world cultivates pandemics.
Hong Kong has a higher density of people living in it than almost any other city
in the world and certainly higher than any city that existed prior to the twentieth
century. Thousands of international flights going to just about any part of the world
you can imagine originate in Hong Kong every day. It also sits a short drive from
the Guangdong province of China. Guangdong houses hundreds of millions of
people and its culinary history includes wild animal delicacies and dishes like pig
organ soup.
The combination of high human population densities, intense livestock produc-
tion, close contact with the diverse microbes of wild animals, and a massive, effi-
cient transportation network gives us a good sense of where the world is heading
with regard to pandemics. Hunters begin the process by capturing wild animals
and bringing them to markets, some of which exist in highly urban areas. The wet
markets, which house live animals, pose particular risks. Once an animal has been
killed, the microbes within it also begin to die, but if a living wild animal makes it
to one of these urban markets, the entire panoply of its microbes are placed
squarely in the midst of large numbers of humans. A virus that gets out here has
definitely won the microbial lottery.
While an interesting example, Guangdong is by no means unique. Regions that
house important wildlife diversity are urbanizing at rapid rates throughout the en-
tire world. Within the past few years, for the first time in human history, we became
a primarily urban species—more than 50 percent of the human population now
lives in urban areas, and that number is growing. By 2050 it has been estimated
that 70 percent of the world’s population will live in cities. And when highly dense
urban populations, the microbes of wild animal and livestock populations, and effi-
cient transportation networks overlap, new diseases will inevitably emerge.
In Africa the particular course of development has provided another set of unique
microbial risks. In central Africa, a region where I lived and worked for a number of
years, the combination of urbanization, deforestation, road building, and con-
sumption of wild game are conspiring to create a recipe for disease emergence.
One of the most common economic activities among the Congo Basin coun-
tries is logging. Unlike the clear-cutting that characterizes logging in some parts of
the world, in central Africa most logging is selective. In selective logging, roads are
cut into the relatively pristine regions with valuable trees, and workers are trans-
ported into them to extract the timber.
Logging in this way has a number of consequences for how viruses emerge.
Among the first things that occur when a new logging camp opens is the large in-
flux of workers. People arrive to clear roads, cut tracks, fell trees, haul trees, cut
them, load them, and manage camps; they all come together to make temporary
towns. The towns consume meat, and since most of the meat consumed in rural
forested regions of central Africa is from wild game, local demand for hunting in-
creases. This attracts more hunters and incentivizes them to hunt more. All of this
serves to increase the number of animals caught and, therefore, the human contact
with the blood, body fluids, and corresponding microbes of the animals present in
these biodiverse habitats.
The existence of logging roads also leads to fundamental changes in the way
that people can hunt. Historically, hunters lived in villages. Their daily hunting
would radiate in a circular fashion from these villages, with decreased impact at the
periphery of the hunting range. Logging roads provide a greater number of points
at which hunters can enter the forest, lay traps, and make kills using firearms. This
has been demonstrated through detailed studies in and around the Campo Ma’an
National Park by the Cameroonian ecologist Germain Ngandjui. At the same time
that forest access is increasing, the movement of trucks along the roads provides
increased routes to urban markets, which in turn increases the number of hunters
who engage in the practice.
Whether from the pressures of the workers themselves or the roads they create,
the practice of logging changes the frequency at which humans have contact with
wild game. The more contact that occurs, the better the chance that a new agent
will jump over. This is compounded by the interconnectivity discussed in chapter
6. The villages are remote, but they are connected by road to major ports, where
the logs (and microbes) can be put on ships and moved throughout the world.
Our work in some of the most rural regions in central Africa provides clear evi-
dence that even seemingly remote places are most definitely on the grid. We regu-
larly screen for potentially pandemic viruses like influenza, and we see evidence of
the globally circulating pandemic H1N1 even in villages in the middle of the forest.
And while we certainly see unusual viruses that are local, we also see cosmopolitan
strains of HIV that have worked their way down the road to infect people living in
distant rural lands. New agents can increasingly get in and out of even the most re-
mote locales.
Sometimes multiple factors accumulate to compound the emerging pandemic
threats. This is exactly what’s happened with the global spread of HIV and its asso-
ciated impact on the human immune system. As we’ve discussed, HIV originally
entered into humans from chimpanzees almost certainly through the hunting and
butchering of these animals by people in central Africa. But now that it’s in human
populations, spreading and infecting such a large number of us, it has the potential
to alter the emergence equation.
Among the terrible consequences of AIDS is that it hampers the immune sys-
tem. In fact, when people die of AIDS, they don’t die of HIV per se. They die be-
cause they eventually succumb to infectious diseases that their immune systems
can no longer control. Approximately 1 percent of the human population worldwide
is immunodeficient. While malnutrition, therapies for cancer, and organ transplan-
tation play a role, the most significant factor is global infection with HIV.
Immunodeficiency leads to the proliferation of a whole range of usual suspects.
Agents like tuberculosis and salmonella multiply more effectively in immunosup-
pressed people. Common agents that aren’t normally deadly can become fatal
when immune systems are weak. Viruses like cytomegalovirus and human her-
pesvirus 8 afflict AIDS sufferers. But immunosuppression can also provide an
entryway for new agents.
Most animal agents don’t come preadapted to humans. Even microbes from
some of our closest relatives often require a combination of genetic changes in
order to be able to survive and spread in a human host. So when a highly exposed
person like a hunter contracts a new agent, the infection will generally be fleeting.
Yet in an immunocompromised host, quickly evolving microbes can often gain
precious time, free of immune pressure, to go through a few more generations of
reproduction, increasing the probability that they will come upon the right suite of
adaptations necessary to take hold in a new species.
And it doesn’t stop there. Sometimes a new virus will cross over into someone
who has been exposed to an animal, but the virus will go nowhere. The existence of
numerous immunosuppressed people in a community will, however, increase the
chance that the virus can begin the process of spreading once it adapts to humans.
Immunosuppression, as caused by HIV or another compromising agent, provides
another foothold for new microbes as they cross the elusive species barrier.
This risk is not trivial. In 2007, along with my colleagues, I reported the results
of a study we’d done in Cameroon to determine the rate of HIV in individuals who
had contact with wild animals through hunting or butchering. We analyzed data
from 191 HIV-infected people living in rural villages near forested settings. The vast
majority of the individuals we studied reported butchering and consuming wild
animals. Over half of the people reported butchering monkeys or apes. Most wor-
rying, 17 of the HIV-positive individuals reported injuries while they’d hunted and
butchered wild animals—perfect opportunities for direct blood-to-blood contact
and bridging of blood-borne microbes.
The fact that people in direct contact with the blood and body fluids of wild ani-
mals also have HIV and may be immunocompromised represents a serious risk for
the emergence of new microbes. Hunting and butchering provide opportunities for
contact with the microbes present in virtually every animal tissue. When these
agents are regularly in contact with people with limited defenses, it may provide a
shortcut for microbes as they traverse the boundaries between species.
Hunting and butchering create serious risks, but even contemporary industrial live-
stock practices, including factory farms and modern meat production, substantially
alter the ways in which we interact with animals in our world. They also increase
the probability that an animal virus will spill over into humans and become a pan-
demic.
Livestock production has changed dramatically over the past forty or so years.
One of the major changes has been raw numbers (so to speak). There are now
more than one billion cattle, one billion pigs, and over twenty billion chickens liv-
ing on our planet. There are estimated to be more domestic animals alive today
than in all the past ten thousand years of domestication through 1960 combined.
Yet this is not simply a numbers game. How the animals are grown and grouped
has also dramatically shifted.
In 1967 the United States had around a million pig farms. As of 2005, the num-
ber had shrunk to a little over one hundred thousand. More pigs and fewer farms
means that more and more pigs are packed together on single large-scale industrial
farms. The same trends exist with other livestock species. In the United States four
massive companies produce over half of the cattle, pigs, and chickens. And this is
not limited to the United States. More than half of the livestock produced globally
now originate in industrial farm settings.
While it’s more economically efficient to grow livestock in industrial settings
there are consequences for microbes. As we’ve seen with humans, larger numbers
of livestock grouped more closely together increases the capacity of livestock pop-
ulations to maintain novel microbes. The animals living on massive industrial
farms largely do not exist in a state of perfect isolation. Contact with blood-feeding
insects, rodents, birds, and bats all provide the opportunity for new agents to enter
into these incredibly massive colonies of animals. When they do, the industrial
farms become far more than settings to grow meat. They become incubators for
infectious agents that could move into human populations. We have seen this
occur with Nipah virus in Malaysian pigs, as discussed in chapter 4. Other viruses
like Japanese encephalitis and influenza can act in similar ways.¹
The number of livestock on the planet now boggles the mind, but the way that
they’re transformed into meat also differs in important ways from how it’s been
done since domestication began. Historically, a single animal would feed a family
or at most a village. With the advent of processed meats, a single hot dog con-
sumed at a baseball game can consist of multiple species (pig, turkey, cattle) and
contain meat derived from hundreds of animals. When you bite into that hot dog,
you’re literally biting into what was only a few decades ago an entire farm.
Combining the meat of many animals and then distributing it to many people
has obvious consequences. Connecting thousands of animals with thousands of
consumers means that an average meat eater today will consume bits of millions
of animals during their lifetimes. What previously was a direct connection between
one animal and one consumer is now a massively interconnected network of ani-
mal parts and those that eat them. And while cooking the meat certainly eliminates
many of the risks, the massive number of interactions increases the potential that a
rogue agent will make the jump.
This is what appears to have happened in the case of the sheep disease scrapie and
bovine spongiform encephalopathy (BSE), better known as mad cow disease. BSE
is among the fascinating group of infectious agents known as prions, mentioned in
chapter 1. Unlike viruses, bacteria, parasites, and any other group of life we know of
on the planet, prions lack the genetic blueprints of biology (i.e., RNA and DNA).
Rather than the combination of genetic material and proteins that make up all other
known life, prions simply have protein. While this may seem insufficient to accom-
plish any organic task, prions are capable of spreading. And they can cause serious
disease.
BSE was first identified as a novel cattle disease in November 1986 because of
the dramatic symptoms it causes in cows. They walk and stand abnormally, and
after some months they experience violent convulsions and death. While there’s
still some debate about its origins in cows, it appears that it came from sheep.
During the 1960s and 1970s as the development of cattle feed was industrialized,
one type of cow feed involved the rendering of sheep carcasses into meat and bone
meal. Sheep have long been known to have a prion disease called scrapie, and it
appears that processing their carcasses as cattle feed permitted the agent to jump
over and adapt.
Once it jumped to cattle, BSE then spread through more feed. Some cattle car-
casses, like sheep carcasses, are also ground into feed for cattle. It appears that
once the prion crossed from sheep to cattle, its primary communication was
through infected cattle meat and bone meal processed for the next generation of
cows.² The spread was remarkably effective. Some have suggested that during this
period more than a million infected cows may have entered into the food chain.
But not all of these prions stayed in cows.
Around ten years after the first identification of BSE, physicians in the UK began
to recognize a fatal neurodegenerative disease among humans who were poten-
tially exposed to contaminated beef. The patients showed evidence of dementia,
severe twitching, and an increasing deterioration of muscle coordination. Evidence
from the patients’ brains revealed that they had been ravaged in exactly the same
ways as those of the cows. Experimental evidence showed that the disease could
also be transmitted to primates whose brains were inoculated with brain tissue
from infected humans. These human patients had been infected with BSE, but
when found in humans, the same disease is called variant Creutzfeldt-Jakob (vCJD)
disease.
While only twenty-four human cases of vCJD have been confirmed to date, there
are certainly others, as the definitive diagnosis is difficult to make. Much is still un-
known about vCJD, but it’s increasingly suspected that infected humans must have
both genetic susceptibility for the deadly brain disorder as well as exposure to in-
fected cow tissue. Analysis of the tonsils and appendixes removed from healthy pa-
tients suggests that as many as one in four thousand people who were exposed
during the UK BSE epidemic are carriers who show no sign of disease. This is par-
ticularly worrying since vCJD has been shown to pass through organ transplan-
tation and may also pass through blood transfusions.
The way that we now grow and distribute meat differs fundamentally from how we
did it in the past. We also transport live animals in new ways. The relative ease of
international shipping means that people can move livestock from regions that
were once remote. And the situation is not unique to animals. Many of our plant
food sources are now transported thousands of miles and eaten by millions before
any microbial contamination related illness would be detected.
In chapter 6 we discussed how monkeypox rates are rising in DRC. But mon-
keypox has not been restricted to Africa. In 2003 monkeypox hit the United States.
Careful investigation of the 2003 US outbreak showed that it emerged from a sin-
gle pet store—Phil’s Pocket Pets of Villa Park, Illinois. On April 9 of that year,
around eight hundred rodents representing nine different species were shipped
from Ghana to Texas. The shipment included six different groups of African ro-
dents, including Gambian giant rats, brush-tailed porcupines, and multiple species
of mice and squirrel. Subsequent testing by the CDC showed that Gambian giant
rats, dormice, and rope squirrels from the shipment were all infected with
monkeypox, which likely spread among the animals during shipment. Some of the
infected Gambian rats ended up in close proximity to prairie dogs at the Illinois pet
store, and those prairie dogs appear to have seeded the human outbreak.
Over the following months there were a total of ninety-three human cases of
monkeypox in six midwestern states and New Jersey. And while most of them
probably resulted from direct contact with infected prairie dogs, some may very
well have resulted from human-to-human transmission.
The moving and mingling of animals as pets and food increases the probability
that new agents will enter into the human population. It also increases the chances
that distinct microbes will end up in the same host and exchange genes. As dis-
cussed earlier, there are multiple ways in which a virus can change genetically: di-
rect changes in genetic information (mutation) or the exchange of genetic infor-
mation (recombination and reassortment). The first option, genetic mutation, pro-
vides an important mechanism for slow and steady production of genetic novelty.
The second options, genetic recombination and reassortment, provide viruses with
the capacity to quickly gain entirely novel genetic identities. When two viruses in-
fect the same host, they have the potential to recombine, exchanging genetic infor-
mation and possibly creating a completely new “mosaic” agent.
This has already occurred to important effect. As we learned in chapter 2, HIV it-
self represents a mosaic virus—two monkey viruses, which at some point infected
a single chimpanzee, recombined and became the ancestral form of HIV. Similarly,
influenza viruses have the capacity to pick up entirely new groups of genes by
forming these mosaics through reassortment, where entire genes are swapped.
Influenza viruses can reassort on the farms where humans, pigs, and birds
interact. Pigs have the potential to acquire some human influenza viruses. They
also can acquire viruses from birds, including wild birds that may pass through on
migration routes. These wild birds can infect pigs directly or indirectly through
domestic birds such as chickens and ducks. When new viruses from birds interact
with human viruses in an animal such as a pig, one of the outcomes is a com-
pletely new influenza virus with some parts from the circulating human virus and
some parts from the bird virus. These new viruses can spread dramatically when
reintroduced into human beings since they can differ sufficiently to avoid detection
by natural antibodies and vaccines from earlier circulating influenza strains.
Recombination plays a potentially vital role in a number of viruses. Genetic
analyses of SARS show that it’s likely a recombinant virus between a bat coron-
avirus and another virus, probably a separate bat virus we have yet to discover.
These two viruses formed a novel recombinant mosaic virus prior to infecting hu-
mans and civets. These viruses’ potential to recombine may very well have related
to the interaction of animals that previously would never have been in contact in
the wild, as they made their way along market networks.
My mentor Don Burke, who now leads the University of Pittsburgh’s School of
Public Health, has played a pivotal role in pointing out how recombination be-
tween viruses can help seed new epidemics. He coined the term emerging genes to
refer to this process. Historically, virologists thought that new epidemics result
from the movement of an entire microbe from an animal to a human. As we’ve
seen in HIV, influenza, and SARS, recombination and reassortment provide other
more stealthy methods to seed new epidemics. Rather than transplant an entire
new microbe, two microbes, one old and one new, can temporarily interact in a sin-
gle host and exchange genetic material. The resulting modified agent may have the
potential to spread and become a completely new, and completely unprepared for,
pandemic. In these cases it’s actually newly swapped genetic information that
causes the pandemic rather than a new microbe—hence the term emerging genes.
In the coming years we’ll see more and more pandemic threats. New infectious
agents will spread and cause disease. New pandemics will emerge as we go deeper
into the rain forests and unleash the agents previously unconnected to interna-
tional transportation networks. These agents will spread as dense population cen-
ters, local culinary practices, and wild-animal trade increasingly intersect. The im-
pact of epidemics will be augmented by HIV-caused immunosuppression that in-
creases the risk of new agents adapting to a damaged human species. As we move
animals quickly and efficiently around the world, they will, in turn, seed new epi-
demics. Microbes that have never encountered each other now will, and they’ll
form new mosaic agents capable of spreading in ways that neither of their parents
could manage. In short, we’ll experience a wave of new epidemics, ones that will
devastate us if we don’t learn to better anticipate and control them.
