THE INTIMATE SPECIES

THE INTIMATE SPECIES

On February 2, 1921, Englishman Arthur Evelyn Liardet went into surgery. Liardet’s 

symptoms were typical, but the surgery was not. At the time of the operation, 

Liardet was seventy-five years old and complained of decreases in his physical and 

mental energy. He had lost most of his hair and had developed wrinkle lines on his 

face. In short, he was growing old. 

Some years before that chilly day in 1921, Liardet had written to an up-and- 

com-ing Russian surgeon practicing in Paris and offered his body for a unique 

procedure. The surgeon, Serge Voronoff, claimed to offer nothing other than total 

bodily rejuvenation—the elixir of life. 

Serge Abrahamovitch Voronoff was born in Russia in 1866. At the age of eigh- 

teen, he immigrated to France, where he studied medicine under the Nobel lau- 

reate Alexis Carrel. Carrel had won his Nobel Prize in 1912 for surgical work on 

blood vessels as well as the new methods of transplantation of both blood vessels 

and whole organs. Carrel taught Voronoff surgery, undoubtedly impressing upon 

him the excitement of science and the potential for discovery, particularly sur- 

rounding the revolutionary new techniques of organ transplantation. In doing so, 

he launched the career of the young, ambitious, six-foot-four Voronoff, described 

in reports as magnetic and imaginative. 

Following his studies with Carrel, Voronoff worked in Egypt for the Egyptian 

king. Voronoff soon became fascinated with the eunuchs that were part of the 

king’s harem. In particular, he noted that the castration they received seemed to in- 

crease the speed at which the eunuchs aged. This observation was the beginning of 

Voronoff’s obsession with a surgical answer to aging. Likely inspired by the pio- 

neering work of his mentor and the excitement of the new surgical techniques, 

Voronoff began to dabble in experimental transplantation. But he went beyond the 

techniques that his mentor had perfected. In early experiments Voronoff trans- 

planted the testicles of a lamb into an old ram, claiming that the transplant served 

to thicken the ram’s wool and increase its sex drive. These early studies fore- 

shadowed the work that would follow.

Some years later, on that cold February day in Paris, Liardet became one of 

Voronoff’s early human experiments. Before Liardet was wheeled into the operating 

room, a chimpanzee had been anesthetized using a specialized “anesthetizing box” 

developed by Voronoff. The box served to protect the technicians from the massive 

and potentially violent male chimpanzees, who would have certainly reacted 

strongly to what was coming. Then Liardet was wheeled in on a gurney and placed 

alongside the chimpanzee. The surgeons carefully removed a testicle from the 

chimpanzee, cut it into thin slices, and grafted pieces onto the testes of Liardet. 

The procedure, known in its day as the monkey gland operation, would go on to 

become remarkably popular. By 1923 forty-three men had received testicles from 

nonhuman primates, and by the end of Voronoff’s career, that number reached the 

thousands. Although Voronoff had inherited a fortune as an heir to a vodka man- 

ufacturer, he made more money operating on many of the most important men of 

his day. Unverified but highly specific accounts point to Anatole France, a Nobel 

Prize–winning French poet as one of his patients. Less reliable rumors suggest 

Pablo Picasso might also have gone under Voronoff’s knife.

But to what end? Many of Voronoff’s patients swore by the procedure. Liardet 

himself claimed to a New York Times reporter in 1922 that the procedure had been 

a huge success. He showed the reporter his strong biceps while his wife nodded 

knowingly by his side. Though the successes claimed by Voronoff and his patients 

were certainly exaggerated, the underlying logic of the procedures remains open to

at least some scientific debate. Voronoff himself, as well as his procedure, even- 

tually fell out of favor with the scientific community. By the time of his death in the 

early 1950s, most considered him a quack, perhaps in part because of the extremes 

to which he went. In the most dramatic of his experiments, he transplanted ovaries 

from a human woman into a female chimpanzee named Nora. He then attempted 

to inseminate her using human sperm!¹ Yet a 1991 editorial on Voronoff in the top 

British medical journal The Lancet concludes with the following words: “Maybe 

medical research councils should fund further research on monkey glands.” 

For our purposes, the utility of the chimpanzee testicle transplants as the Viagra of 

the roaring twenties, while interesting, is largely unimportant. What’s important 

about the infamous monkey gland operation is that it provides one of the most 

striking examples of how medical technologies have incidentally served to link hu- 

mans (and sometimes animals) in ways that create new bridges for the movement 

of microbes. 

Given what we now know, the idea that we would consciously connect the 

microbial worlds of humans and chimpanzees as Voronoff did would be unfath- 

omable and unforgivable. Although there’s no straightforward way to confirm it in 

the absence of specimens, Voronoff’s transplants almost certainly led to the trans- 

mission of potentially dangerous viruses into humans who received these tissues. 

Transplanting living tissue between very closely related animals eliminates all of 

the natural “barriers to entry” that microbes face, and remains one of the riskiest 

imaginable ways for a microbe to jump from one species to the next. 

Yet Voronoff’s work, while certainly extreme, did not exist in a vacuum. The 

explosion of medical technologies that has occurred over the past four hundred 

years has provided new kinds of microbial connections between individuals. Trans- 

fusion, transplantation, and injection, while some of the most critical tools for 

maintaining human health, have also contributed fundamentally to the trans- 

mission and emergence of pandemics. These technologies have connected us with 

one another’s blood, organs, and other tissues in ways unprecedented in the his- 

tory of life on our planet. They have served to make us, among other things, the 

intimate species.

Before we dissect the role of medical technology in connecting our bodies and fa- 

cilitating microbial transmission, it’s worth spending a moment to discuss this in 

the context of the benefits of these technologies. Injections and immunizations as 

well as transfusions and transplants are all technologies that have catapulted 

medicine into the modern age. 

Without blood transfusions, huge numbers of hemophiliacs, trauma victims, 

and wounded soldiers would die. Transplants permit victims of leukemia, hepatitis, 

and severe burns to live a normal life. And it is nearly impossible to imagine a 

world without injections. The use of intravenous rehydrating fluids alone saves the 

lives of millions of malnourished children and victims of diarrheal disease each 

and every year. Injections also permit immunization, and to live in a world without 

immunizations is to live in a world where smallpox threatens our day-to-day lives. 

If smallpox had not been eliminated by immunization in the 1960s, it would prob- 

ably be a worse plague today than it was then due to the same sort of hypercon- 

nectivity discussed in chapter 6. 

Examining the role that these medical technologies have played in the history of 

epidemics does not argue against their utility in maintaining the health of our 

species. Likewise, these arguments should not be interpreted as supporting the 

hypochondriacal fears of the anti-immunizationists, whose rhetoric has been 

soundly skewered in Michael Specter’s important book, Denialism, which brings to 

a general audience years of research on the subject. Nevertheless, understanding 

the ways in which the historical use of these technologies has connected human 

populations is important in understanding why we are plagued with pandemics. 

Rather than discourage us from using live-saving technologies, they serve to high- 

light the need for maintaining vigilance in the way that we deploy them. 

One of the clearest examples of how medical technology increases human micro- 

bial interconnectivity is our use of blood. Historically, humans (and other animals) 

rarely come into contact with one another’s blood. For the vast majority of our his- 

tory since the advent of hunting, we’ve had more contact with the blood and body 

fluids of other animals, through hunting and butchering. In the fifteenth century,

that would all change. 

The first generally accepted attempt at a “blood transfusion” was given to Pope 

Innocent VIII in 1492 and was described by the historian Stefano Infessura.² When 

the pope went into a coma, the pontiff’s medical advisers sought to cure him by 

feeding him the blood of three ten-year-old boys. At the time, there were no intra- 

venous techniques, and both the pope along with the three donors, who had been 

promised a ducat each, all died.³ 

Blood transfusions have advanced considerably since then. Today around 

eighty million units of blood are collected every year worldwide. Blood transfusions 

save countless lives. They also provide an entirely new form of connection between 

human populations. When a unit of blood is transfused from individual to indi- 

vidual, so too are the various viruses and other microbes present in that unit. The 

proliferation of blood transfusions creates a novel route for the movement of mi- 

crobes, sometimes providing a new route for microbes that already move in other 

ways, as in the case of malaria. New connections made through medical tech- 

nology can also provide transmission routes for agents that would otherwise never 

have the potential to spread among humans and can be another way in which an 

agent that we acquire from an animal can spread; otherwise, it might simply go ex- 

tinct. 

Blood transfusions are known to spread HIV and other retroviruses, as well as 

hepatitis B and C, parasites such as malaria, and Chagas disease. Even prions like 

variant Creutzfeld-Jakob (also known as mad cow disease), an infectious agent to 

which we’ll return in the next chapter, can survive in blood bags, the plastic con- 

tainers used to hold blood prior to transfusion. 

The field of blood products has also advanced beyond single blood trans- 

fusions that go from one person to the next. In the case of hemophiliacs, indi- 

viduals lack particular blood factors that would normally allow their blood to clot, a 

potentially life-threatening condition. In order to accumulate the missing blood fac- 

tors in sufficient quantities to solve the problem, the appropriate components of 

blood are often pooled from tens of thousands of donors. The consequences for 

connectivity are substantial. A back-of-the-envelope calculation suggests that a per- 

son living with hemophilia A in a city like San Francisco will inject themselves with 

up to 7,500 doses of clotting factor VIII by the time that they’re sixty. That means 

that this person will potentially have had contact with the blood-borne microbes of

2.5 million people during the course of their lifetime. 

The good news is that many blood banks now screen for the usual suspects. 

Blood infected with HIV, for example, will not get through the donation process.⁴ 

But this was not always the case. Perhaps not surprisingly, hemophiliacs who re- 

ceive pooled blood products were among the first found to be infected with HIV in 

the early 1980s. In the United States alone, thousands of hemophiliacs were in- 

fected, and many of them died. Even now we can only screen for the microbes we 

know. Undiscovered viruses, of which there are certainly many, move around daily 

through blood products. And a new virus that entered into humans could easily 

spread within the blood supply before we’d have a chance to stop it. 

In terms of sheer number of procedures, blood transfusions trump organ trans- 

plants by far. But while the number of blood transfusions will always be greater 

than the number of organ transplants, the movement of an organ is a substantially 

more dramatic biological event. Organ transplantation involves the movement of 

blood as well as a large amount of tissue, so any microbes present in the blood or 

the tissue being transplanted will move along with the organ into the recipient. 

Organ donation risks the movement of all of the same usual suspects that will 

transmit during a blood transfusion and then some. For example, in the case of ra- 

bies, discussed in detail in chapter 5, I told you that rabies didn’t transmit from 

human to human. To be slightly more exact, there have been no documented cases 

of natural transmission of rabies from human to human. There have, however, 

been a dozen or so well-documented cases of rabies moving from one person to 

another. And every one of them has been due to a transplant with an infected 

organ. 

The majority of these cases of rabies transmission have been due to cornea 

transplants, perhaps because the cornea is one of the only nervous system-related 

tissues currently transplanted; and rabies is primarily a virus of the central nervous 

system. In two fascinating cases, separate recipients from Texas and Germany re- 

ceived organs infected with rabies. In both cases the deaths of the donors were 

falsely attributed to drug overdoses, whose symptoms can sometimes mimic those 

of rabies. Amazingly, both donors appeared to have died of fulminant rabies with- 

out seeking medical care. It’s frightening to imagine that they reached that point in

the illness while moving about, conducting their normal day-to-day affairs. 

Transplants can also transmit dormant stages of infectious diseases that can 

flare up later. One particular species of malaria, Plasmodium vivax, whose Siberian 

variant we discussed in chapter 1, has the capacity to stay latent, or dormant, in the 

liver. During latency, there are no symptoms of the disease and, similarly, no 

malaria parasites in the blood. But a liver transplant could potentially do the trick. 

In one case in Germany, a twenty-year-old male who had emigrated from 

Cameroon died of a brain hemorrhage and donated his organs. Among the recip- 

ients was a sixty-two-year-old woman who needed the liver because of late-stage 

cirrhosis. A full month after her organ transplant she developed a high-grade fever, 

which was later diagnosed as vivax malaria and successfully treated. She had never 

visited a tropical or subtropical area in her lifetime. But her liver had. 

There’s another important rub to the problem of organ transplantation. While ob- 

taining blood from donors is pretty simple, obtaining an organ is not. Rarely will 

people living in the developed world who need a blood transfusion not get one, but 

that is not the case with organ transplants. Currently in the United States there are 

approximately 110,000 people on the waiting list to receive organ transplants, and 

one of these people dies every ninety minutes. 

The lack of organs available for transplant has caused surgeons to look for alter- 

natives to human organs. Animals are an obvious choice. Clearly, the elective 

transplantation of thousands of chimpanzee testicles into men for the purposes of 

“rejuvenation” presents unacceptable risks. The real chance that a known or un- 

known virus could enter into humans from such a closely related animal as a chim- 

panzee would make the choice wrong even if the illness were life-threatening. But 

there are other animals out there. For example, the organs of an adult pig are ap- 

proximately the size and weight of an adult human’s, and while not without risk for 

cross-species jumps, the risks are smaller than those for a chimpanzee. 

In July 2007, Joe Tector, a pioneering transplant surgeon at Indiana University 

School of Medicine, gave me a call. Tector had put together a team whose goal was 

to genetically engineer pigs with organs that would be less likely to be rejected by 

humans, a problem for surgeons to this day. Within five years he wanted to begin 

transplanting pig livers into humans, and he wanted to understand the risks.

He explained that he didn’t want a rubber stamp scientist to simply tell him that 

what he was doing was safe. He was looking for someone who loved finding new 

viruses and was intent on discovering any possible risk associated with the work 

he was doing. He spoke eloquently about his patients and how many of the people 

on those waiting lists never received organs in time. He also spoke about the need 

to determine that what he planned to do wouldn’t backfire, igniting a new pan- 

demic in the human species. When Tector contacted me, I had already been inter- 

ested for some years in xenotransplantation, the surgical term for the transplan- 

tation of organs from one species to another. By the time I got off the phone, I was 

hooked. 

In the 1920s, following the time that Voronoff conducted his work in Paris, the 

field of xenotransplantation went into a forty-year lull during which there were no 

documented attempts. But in the 1960s work on xenotransplantation had a rebirth. 

New antibiotics and immunosuppressive drugs provided hope for the success of 

transplanting major animal organs into people who needed them. By dampening 

the immune system, the immunosuppressive drugs could address the frustration 

of organ rejection. 

A series of high-profile operations brought major attention to the field through 

the 1980s. One involved the famous Baby Fae, a twelve-day-old baby girl born 

prematurely with a major heart disorder. She survived for eleven days on a baboon 

heart. Another operation created a news flurry around Jeff Getty, a thirty-eight- 

year-old man with AIDS. Getty received his diagnosis at a time when AIDS was still 

called “gay cancer.” He went on to become a prominent activist who pushed for 

access to care for AIDS patients and participated in numerous experimental trials, 

including the one that led to his national notoriety. In the trial, he received a bone 

marrow transfusion from a baboon with the hope that the natural resistance that 

baboons have to AIDS would take hold in his body. 

Getty’s experimental therapy ultimately failed, but it brought with it a national 

debate about the potential that such transplants could transmit new and perhaps 

unknown viruses to humans. Certainly, a transplant from a closely related species 

like a baboon to a person with an already compromised immune system could be a 

recipe for disaster. A person with a highly weakened immune system, as occurs in 

late stages of AIDS, would provide an environment in which new viruses could bet- 

ter grow and adapt.⁵ In the extreme, it could be a Petri dish for viral exploration into

a new and foreign land. 

Fortunately for the success of Tector’s work, pigs are not as closely related to 

humans as baboons are. Yet they are still mammals. As with other mammals (in- 

cluding ourselves), they have many microbes that are still unknown. And some of 

them undoubtedly have the potential to jump species. The real question then be- 

comes what are the viruses that can jump and can they then spread from person to 

person. The fact that one person might get a deadly virus is not the end of the 

world, particularly if the person was about to die of liver failure. The real risk is if 

that virus could spread. 

In the small but active group that concern themselves with pig viruses, the 

agent that has provoked the most worry is PERV, the porcine endogenous retro- 

virus. Endogenous viruses like PERV are permanently integrated into the genetic 

material of their hosts. Yet from time to time they emerge from the genes and go 

on to infect cells and spread within the host’s body. As part of the actual genomes 

of their hosts, endogenous viruses cannot currently be eliminated—hence the con- 

cern that they could reemerge in humans following a pig transplant. 

The eminent CDC virologist Bill Switzer, whom I’ve worked closely with for the 

last ten years studying retroviruses, was one of the scientists to conduct the most 

comprehensive study on PERV in xenotransplant recipients. Bill and his colleagues 

studied specimens from 160 patients who had received pig tissues. Amazingly, 

they found evidence of pig cells continuing to live in about 15 percent of the recip- 

ients, even up to eight years after the transplant. Fortunately, they found no evi- 

dence of PERV. 

Whether PERV is the most important risk or not remains unknown. If it is, we 

may not have much to worry about. Through our studies with Tector and other col- 

leagues, we hope to determine what else may be in those pig tissues and what risks 

those agents would pose. The decisions based on our research will not be easy 

ones. As we’ll discuss further in chapter 9, even state of the art viral discovery right 

now does not permit us to definitively determine all of the microbes in any sample. 

Yet the costs of indecision are substantial. On one side are the transplant recip- 

ients who die each day waiting for an organ. On the other is a small but important 

risk of an epidemic in a much larger group. Is one life saved worth a species poten- 

tially plagued?

We’ve been sticking ourselves with needles for a long time. The first evidence of it 

comes from an unusual source—an iceman. On a sunny day in September 1991, 

two German tourists hiking in the Italian Alps came across a corpse. The corpse 

became known as Ötzi, after the valley in which he was discovered. Though initially 

thought to have died recently, we now know that Ötzi lived 5,300 years ago. 

Among the amazing elements of this discovery is the fact that Ötzi had tattoos. 

In fact, this is the first evidence of tattoos in the world. Ötzi’s tattoos were located 

on his lower back, ankles, and knee. X-rays of the mummy showed evidence that 

the tattoos were positioned over spots where Ötzi had likely experienced pain due 

to orthopedic maladies, leading some to speculate that the tattoos may have 

served as a kind of therapy. 

Whatever his reasons for having them, Ötzi’s tattoos, like any tattoo since, 

represent risks. Tattooing, like a needle stick or an injection, involves blood con- 

tact. And if the same implement is used multiple times on different individuals, it 

can provide a bridge on which microbes can hop hosts.

Whether for tattoos, medicines, or vaccines, improperly sterilized needles can

play an important role in transmitting microbes. Widespread use of needles, as 

with blood transfusions, provides an entirely novel route for microbes to move 

around, allowing them to maintain themselves or spread effectively in humans in 

order to survive and thrive. 

Perhaps the most remarkable microbe we know of in the postinjection age is hep- 

atitis C virus. HCV is a critically important virus that infects over one hundred mil- 

lion people globally and more than three million new individuals each year. It also 

kills through liver cancer and cirrhosis, causing over eight thousand deaths per 

year in the United States alone. But it would likely kill precious few of those indi- 

viduals if it weren’t for needles. 

There is still a great deal that’s unknown about HCV. The virus itself was offi- 

cially discovered in 1989, but it must have been in human populations for much 

longer. My collaborator, the prolific Oxford virologist Oliver Pybus, has made 

understanding this virus one of his many scientific objectives. Pybus utilizes the 

tools of evolutionary biology and learns more each year about viruses through 

computers than many others will in a lifetime of lab- or fieldwork. By using com- 

puter algorithms to compare genetic information from distinct viruses as well as 

mathematical modeling, Pybus has made some fascinating discoveries about HCV. 

What we do know about HCV is that it’s on the move. During the past hundred 

years, the virus has spread rapidly through blood transfusions, the use of unster- 

ilized needles to deliver medicines, and through injection drug use. But genetic 

analyses by Pybus and others have shown that the virus is somewhere between five 

hundred and two thousand years old, so these contemporary technologies likely do 

not tell the whole story. Essentially, it seems there were places, most likely in Africa 

and Asia, where HCV existed on a much smaller scale prior to the massive expan- 

sion that needles and injections permitted. 

Since HCV is not effectively transmitted sexually or by normal contact between 

people, other routes of transmission must somehow explain how it persisted many 

centuries ago. The virus can be transmitted from mother to offspring, but that too 

is an unlikely explanation since so-called vertical transmission is not particularly 

efficient. Certainly, cultural practices like circumcision, tattooing, ritual scarifi- 

cation, and acupuncture probably played a role. In an interesting twist, Pybus and

his colleagues have used a combination of geographic information systems (to 

which we’ll return in chapter 10) and mathematical models of disease spread to 

show that another possibility would be some kinds of blood-feeding insects. These 

insects could have contributed to historical transmission by acting as natural con- 

taminated needle sticks and carrying virus-infected blood from one host to the next 

on their mouthparts. 

Unsafe injection practices contributed to the spread of much more than HCV in 

the twentieth century. In a series of thoughtful articles, the Tulane virologist Pre- 

ston Marx and his colleagues have argued that injections helped launch the HIV 

pandemic. Some mysteries still persist on the early spread of HIV. While the ge- 

netic data points to an early twentieth-century jump of the chimpanzee virus that 

would become HIV, understanding what sparked its true global spread in the 

1960s and 1970s remains up for debate. For many scientists, the expanding air 

routes discussed in chapter 6 are sufficient to explain this phenomenon. But Marx 

and his colleagues add another potential cause. 

The period that coincides with the global spread of HIV also coincided with a 

dramatic expansion in the availability of cheap injection systems. Prior to the 

1950s, syringes were handmade and relatively expensive. But in 1950 machines 

began churning out glass and metal syringes, and in the 1960s disposable plastic 

syringes became available. Effective ways to inject drugs and vaccines contributed 

to the increased use of injections for medications and vaccines in the late nine- 

teenth century. Often medical campaigns used the same unsterilized needle to 

vaccinate hundreds or more individuals at a time, setting up unique conditions that 

could potentially launch epidemics.⁶ An individual hunter who had been infected 

with a virus from a hunted chimpanzee could theoretically transmit that virus to 

many other individuals in just this way, the conditions under which Marx and his 

colleagues think that the global launch of HIV began in earnest.

It’s important to note that Marx’s work is distinct from the oral polio vaccine hy- 

pothesis for HIV origins that appeared first in a Rolling Stone article in 1992. Marx 

and his colleagues suggest that unsafe injection practices helped to spread HIV; 

they do not, however, argue that these techniques contributed to its introduction 

from chimpanzees to humans. Alternately, the OPV hypothesis argued that since 

oral polio vaccine was grown on fresh primate tissues HIV jumped directly from 

such tissues to vaccines and spread as they were administered. 

The OPV hypothesis is no longer taken seriously by the scientific community for 

four primary reasons: (1) retrospective analysis of the original vaccine stocks 

showed no evidence they were infected by the chimpanzee virus that seeded 

human HIV; (2) genetic analyses suggest HIV has been around for roughly one 

hundred years, far predating the period of OPV use; (3) the chimpanzee strains in 

the region where the purportedly contaminated vaccine stocks were produced are 

distinct from the chimpanzee virus that seeded HIV; (4) the pervasive human 

exposure to these viruses through hunting and butchering of wild primates pro- 

vides a more parsimonious explanation for the distribution of the multiple primate 

viruses in the HIV family that have crossed into humans. 

Further highlighting the end to the OPV debate in 2001, four separate articles 

published in the leading scientific journals Nature and Science laid it to rest. Doing 

so was important for a number of reasons, including the fact that the hypothesis 

was misinterpreted in a way that severely compromised ongoing vaccine

campaigns, which use vaccines that are universally acknowledged as both safe and 

effective. An accompanying editorial to the Nature articles sums it up well: “The 

new data may not convince the hardened conspiracy theorist who thinks that con- 

tamination of OPV by chimpanzee virus was subsequently and deliberately covered 

up. But those of us who were formerly willing to give some credence to the OPV 

hypothesis will now consider that the matter has been laid to rest.” More blunt 

were the words of my colleague Eddie Holmes, one of the world’s most distin- 

guished virologists, who said, “[The] evidence was always flimsy, and now it’s 

untenable. It’s time to move on.” 

While unsafe injections may very well have contributed to HIV’s spread, as they 

did with HCV, they did not lead to its introduction. This, however, doesn’t mean 

that we should ignore vaccine safety. 

Right now around one in fifteen individuals reading this book are infected with a 

virus that jumped into them from a monkey. To be more specific, if you’re one of 

these individuals, you’re infected with SV40, a virus of Asian macaques, and you 

acquired it from a contaminated vaccine. 

During the 1950s and 1960s, poliovirus vaccines were grown on cell cultures 

derived from macaque kidneys. Some of these kidneys were infected with SV40, 

which then contaminated the vaccines. The results were dramatic. 

In the United States alone, up to 30 percent of the poliovirus vaccines in 1960 

were contaminated with the virus. From 1955 through 1963, roughly 90 percent of 

American children and 60 percent of American adults were potentially exposed to 

SV40—an estimated ninety-eight million people. And the virus is not a trivial one. 

It causes cancer in rodents and can make human cells living in laboratory cell cul- 

ture reproduce abnormally, a worrying sign that they may have the potential to 

cause cancer. 

The idea that more than half of the American population was placed at risk from 

infection with a novel monkey virus had a notable effect on science, and epidemi- 

ologists scrambled to determine if the individuals who’d received the virus had 

cancer. Fortunately, while the evidence is still debated to this day, it appears clear 

that SV40 did not pose a serious risk for cancer and, perhaps even more impor- 

tantly, it didn’t have the potential to spread. We dodged a major bullet.

But because a single vaccine stock can be administered to thousands of indi- 

viduals, we must remain vigilant. Contamination of a vaccine stock or multiple vac- 

cine stocks can contribute to millions of infections with new viruses, just as we 

witnessed in the 1950s and 1960s with SV40. This does not mean that vaccines are 

not safe. They are! And they are essential to protect billions of people all over the 

globe. Health monitoring and vigilance in vaccine production has also never been 

greater. In a recent and important study, my collaborator Eric Delwart, a San Fran- 

cisco–based scientist who perfects techniques to discover unknown viruses, 

showed that some of these new approaches, which we’ll discuss in chapter 10, can 

be applied to even further increase the safety of vaccines. The risks associated with 

current vaccines are substantively less than the risks associated with the diseases 

they protect against. Yet the risks are not zero. We must make sure that when we 

knowingly connect animal and human tissues—particularly on an industrial 

scale—we do so with the utmost care. 

Since the 1920s when Voronoff conducted his monkey gland operations, our 

planet has witnessed an explosion in the use of transfusions, transplants, and 

injections. These wonderful technologies have helped rid us of some of our dead- 

liest diseases. Yet they have also provided powerful new biological connections be- 

tween individuals, which sometimes serve as an unwelcome by-product of these 

beneficial tools. They provide bridges on which microbes can move, bridges that 

did not exist until now. They pull humans together into a completely new kind of 

intimate species, one unique to life on our planet and one that fundamentally 

changes our relationship with the microbes in our world.

ONE WORLD

ONE WORLD 

In 1998 scientists working independently in Australia and Central America an- 

nounced that they were finding massive numbers of dead frogs in the forests 

where they worked. The large-scale die-off was especially dramatic. Global amphib- 

ian populations had been declining for some time, but these mounting frog deaths 

occurred in pristine habitats—places far less likely to have been exposed to toxic 

by-products of human cities or other man-made environmental threats. Field biolo- 

gists and tourists alike witnessed the large numbers of dead frogs scattered about 

the forest floor. This was rare indeed since scavengers quickly eat dead animals. To 

see so many indicated that the predators already had their fill of free frogs and 

these were the leftovers. In fact, it was just the tip of the iceberg. A massive and un- 

precedented amphibian carnage was under way. 

The expiring frogs all displayed similar and worrying symptoms. They became 

lethargic, their skin sloughed off, and they often lost their ability to right them- 

selves if turned over. In the months that followed the first announcements, a 

number of possible explanations came forth—pollution, ultraviolet light, and dis- 

ease among them. Yet the particular pattern of death was most consistent with an 

infectious agent. Animal deaths spread in wavelike patterns from one location to 

the next suggesting the spread of a microbe, a contagion sweeping through the 

Central American and Australian frog world.

The solution to the mystery came in July 1998, when an international team of 

scientists reported the source of the frog disease. The team found evidence that a 

majority of the frog species succumbing to the die-offs were infected with a partic- 

ular species of fungus. The fungus they identified was Batrachochytrium 

dendrobatidis, known more simply as the chytrid fungus (pronounced KIT-rid). 

They found evidence of chytrid, which had previously been seen exclusively in in- 

sects and on decaying vegetation, on a number of dead frogs. Tellingly, when they 

scraped the fungus from the dead and infected healthy laboratory tadpoles with it, 

they were able to re-create the fatal symptoms. The fungus was to blame. 

Since the 1998 report, this fungus is now documented on all continents that 

have frog populations. It can survive at sea level but also wreaks havoc at altitudes 

up to twenty thousand feet. And it’s a killer. In Latin America alone, chytrid fungus 

has been linked to extinction in 30 of the 113 species of the strikingly beautiful 

harlequin toads. Thirty species forever removed from the biological diversity of our 

planet. 

While the spread and devastation of chytrid has now been well documented, 

much about it remains unknown. The large-scale declines in amphibian 

populations predated the emergence of the fungus, so it is not the only problem 

that is devastating global frog populations, but it’s definitely among them. Another 

key factor is the steady decline in available frog habitat as the human footprint has 

increased over the last hundred years. 

The questions of where the fungus originated and how it spreads are largely 

outstanding. Work done on archived specimens from South Africa shows that the 

fungus has infected African frogs since at least the 1930s, decades before it hit any 

other continent. This points to an African origin. Yet at some time, the fungus 

spread and did so quite effectively. How did it manage to get so cosmopolitan so 

quickly? 

One possibility is the exportation of frogs. The researchers who discovered the 

early evidence of chytrid in South Africa also noted that some of the species of the 

frogs infected were commonly used in human pregnancy tests. When injected by 

lab technicians with urine from pregnant women, African clawed frogs (Xenopus 

laevis) ovulate—which made for an early, if significantly more cumbersome, ver- 

sion of the common pregnancy dipsticks used today! Following the discovery of 

this human pregnancy test in the early 1930s, thousands of these frogs were

transported internationally for this purpose. Perhaps they took chytrid fungus with 

them. 

But Xenopus was likely not alone in causing the global spread; since one stage of 

the fungus’s life cycle actively spread in water, that was also a probable factor. 

Human movement almost certainly played a role as well. Our shoes and boots are 

at least partially to blame. This small fungus, wanted in the deaths of frogs world- 

wide, hijacked us. 

The chytrid fungus has resulted in global frog deaths and in some cases extinc- 

tion of entire frog species, a tragic loss for wildlife on our planet. In a 2007 paper, 

Lee Berger, one of the researchers who first identified the chytrid fungus, used lan- 

guage uncommon in conservative scientific journal articles when he wrote, “The 

impact of [chytrid fungus] on frogs is the most spectacular loss of vertebrate biodi- 

versity due to disease in recorded history.” 

What happened with the chytrid fungus also gives us important clues to a larger 

phenomenon that affects much more than just amphibians. Over the past few hun- 

dred years, humans have constructed a radically interconnected world—a world in 

which frogs living in one place are shipped to locations where they’ve never 

previously existed, and one where humans can literally have their boots in the mud 

of Australia one day and in the rivers of the Amazon the next. This radically mobile 

world gives infectious agents like chytrid a truly global stage on which to act. We 

no longer live on a planet where pockets of life persist for centuries without contact 

with others. We now live on a microbially unified planet. For better or worse, it’s 

one world. 

  

How did we get to this point? For the vast majority of our history as living organ- 

isms on this planet, we had incredibly limited capacity to move. Many organisms 

can move themselves over short distances. Single-celled organisms like bacteria 

have small whiplike tails, or flagella, that allow them to move, but despite their 

molecular-scale efficiency, flagella will never push their owners far. Plants and 

fungi have the potential to move passively by creating seeds or spores blown by 

the wind. They also have adopted methods that co-opt animals to help them move, 

which explains the existence of fruit and the spores of fungi like chytrid. Never- 

theless, precious few forms of terrestrial life regularly travel more than a few miles

in the course of their lives. 

Among the wonderful exceptions to the largely static life on Earth is the coconut 

palm. The seeds of the coconut palm (i.e., coconuts), like a number of other drift 

seeds, evolved buoyancy and water resistance, permitting them to travel vast dis- 

tances through ocean currents. Among animals, some species of bats and birds 

are masters of space. The best example might be the Arctic tern, perhaps the most 

mobile species on Earth outside of our own. The tern flies from its breeding 

grounds in the Arctic to the Antarctic and then back again each and every year of its 

life. A famous tern chick was tagged on the Farne Islands in the UK near the time it 

was born in the summer of 1982. When it was found in Melbourne, Australia, in 

October of the same year, it had managed a twelve-thousand-mile journey in the 

first few months of life! It’s been estimated that these amazing birds, which can 

live over twenty years, will travel about one and a half million miles in their life- 

times. It would take a full-time commercial jet pilot, flying at the maximum FAA 

permitted effort, nearly five years to cover the same distance. 

Yet despite their wings, most bird and bat species actually live their lives quite 

close to where they’re born. Only a few, like the Arctic tern, have evolved to 

regularly move great distances. Highly mobile species, whether bird, bat, or 

human, particularly the ones that live in large colonies, are of particular interest for 

the maintenance and spread of microbes. Among primates, only humans have the 

potential to move themselves great distances during a single lifetime, let alone in a 

few days. That’s not to say that other primates simply stay put. Almost all species 

of primates move every day in their search for food, and young adults routinely 

move from one area to another before mating. Yet whether primate or bird, nothing 

on the planet—certainly nothing outside of the sea—matches humans in our 

capacity to move long distances quickly. The human potential to move, which now 

includes traveling to the moon, is unique and unprecedented in the history of life 

on our planet. But it comes with consequences. 

Humans started globetrotting in earnest millions of years ago using our own two 

feet. Bipedalism gave us an advantage over our ape cousins in terms of our capac- 

ity to wander. And, as discussed in chapter 3, it had consequences for how we 

interact with the microbes in our environment. Yet our capacity to negotiate the

globe in the amazing way we do now started with our use of boats. 

The earliest clear archaeological evidence of boats dates to around ten thou- 

sand years ago. Found in the Netherlands and France, these boats (which might be 

better called rafts since they were made by binding logs together) were probably 

used primarily in fresh water. The first evidence of sea-going boats comes from a 

group of British and Kuwaiti archaeologists, who in 2002 reported finding a seven- 

thousand-year-old vessel that undoubtedly was used at sea. The archaeologists 

made their discovery at the Neolithic site of Subiya in Kuwait. Stored in the rem- 

nants of a stone building, the boat consisted of reeds and tar. Most strikingly, the 

bits of boat had barnacles attached to the tar, indicating that it was definitely used 

in the sea. 

Employing genetics and geography, we can get a much earlier estimate for the 

first use of seafaring boats. The indigenous people of Australia and Papua New 

Guinea provide perhaps the best case for this. By comparing the genes of the Aus- 

tralasian people with other humans throughout the world, we can conclude that 

people reached Australia at least fifty thousand years ago. 

During this time, our planet was a relatively cold place—it was the peak of an 

ice age. Since more of the Earth’s water was locked up in ice, the sea level was 

lower, revealing pieces of land that connected what are currently islands. Many of 

the islands in the Indonesian archipelago were joined by these so-called land 

bridges. 

Despite the land bridges that ice ages expose, we know that no one walked all 

the way to Australia. In particular, the deep-water channel between Bali and Lom- 

bok in present-day Indonesia, a channel around thirty-five kilometers long, would 

have required boats to navigate. So we can infer that these early populations also 

used at least some form of sea transport. 

We know very little about these early Australian settlers, although we know that 

they traveled at a time before animal domestication so certainly didn’t move with 

animals in tow. Nevertheless, their movements impacted how they related with mi- 

crobes. When they first crossed from Bali to Lombok, they encountered a com- 

pletely novel set of animals. 

The channel between Bali and Lombok lies squarely on Wallace’s Line, the fa- 

mous geographic divide named after the nineteenth-century British biologist Alfred 

Russel Wallace who, along with Charles Darwin, codiscovered natural selection.¹ 

While the distance between Bali and Lombok was no greater than that between 

many of the waterways separating the hundreds of islands along the Indonesian 

archipelago, Wallace noted that animal populations on either side of the channel 

differed extensively. And while he didn’t have the precise models for ice age water 

levels that we have today, he surmised that this biological divide existed because 

Bali and Lombok were never connected by a land bridge, something we now know 

to be true. 

Like humans, other animals take advantage of land bridges, but unlike these 

earlier settlers who had boats, the animal populations that couldn’t fly long dis- 

tances were largely stuck on one or another side of this deep-water barrier. When 

the first explorers left Asia for the Australasian continent, making the thirty-five- 

kilo-meter hop from Bali to Lombok, they took a fairly short trip by boat but a huge 

leap for primates. When they crossed this divide, these early explorers entered a 

world that had never seen monkeys or apes before. They also encountered com- 

pletely new microbes.

limited, since the small population sizes of the settlers wouldn’t have been able to 

sustain many kinds of agents. 

It’s hard to know exactly what the first trips across Wallace’s Line were like. 

They may have been colonization events with small groups that were then com- 

pletely cut off. Perhaps more likely they were short initial forays into new lands, fol- 

lowed by the establishment of temporary outposts, much as we consider colo- 

nizing the moon. The actual way in which the new lands were colonized would 

have played an important role in determining the flow of microbes in either direc- 

tion. And while these first Australasian humans almost certainly had some connec- 

tions to the “mainlanders” they left behind on Bali, that contact may have been very 

infrequent. Yet some new Australasian infections that had the potential for long- 

lasting human infection could very well have made their first forays into human 

populations on the Asian side of the divide. 

The use of boats to visit new lands would continue with increasing frequency over 

the forty or so thousand years following this first colonization of Australasia. We 

have much better knowledge of what later trips were like and how they connected 

microbially distant lands. Perhaps the peak of boating-based colonization before 

modern times occurred among the Polynesian populations of the South Pacific. 

Among these Polynesian journeys, probably the most incredible was the first 

discovery of Hawaii, over two thousand years ago.² For the first lucky settlers, find- 

ing this island would have been truly like finding a needle in a haystack. To give a 

sense of scale, the largest island of the Hawaiian archipelago, also named Hawaii, 

has a diameter of around a hundred miles. And the Southern Marquesas, whose 

inhabitants were the most likely first colonizers of Hawaii, are some five thousand 

miles away. To imagine what it would have been like to hit the mark, imagine we 

blindfolded an Olympic archer, then spun him around and asked him to hit his tar- 

get—the ratios are about the same. One can only imagine how many boats (and 

their inhabitants) were lost before the fortunate finally made it. 

On their long trips, the Polynesians probably lived largely on caught fish and 

rainwater. Yet they traveled with a veritable biological menagerie. They brought 

along sweet potatoes, breadfruit, bananas, sugarcane, and yams. They also traveled 

with pigs, dogs, chickens, and probably (unintentionally) rats. Having all of these

domesticated species meant that the flotillas carried not only life support for the 

Polynesian explorers, but also minirepositories of microbes, which would spread 

and mix with local microbes in the places that they discovered. 

The boat journeys of the Polynesians, as remarkable as they were for their time, 

pale in comparison to the global shipping that emerged in the fifteenth and six- 

teenth centuries. By the time Europeans reached the New World, in the late fif- 

teenth century, thousands of massive sailing ships were plying the waters of the At- 

lantic and Indian Oceans and the Mediterranean Sea, moving people, animals, and 

goods back and forth between the countries of the Old World. 

The impact of smallpox on New World populations is the most dramatic known 

example of the way that the connections formed by shipping can influence the 

spread of microbes. Some estimates suggest that as many as 90 percent of the 

people living in the Aztec, Maya, and Inca civilizations were killed by smallpox 

brought by boats during European colonization, a massive and devastating car- 

nage. And smallpox was only one of many microbes that spread along the shipping 

routes of this time. 

Each of the major transportation advances would alter connectivity between 

populations, and each would have their own impact on the spread of new mi- 

crobes. The exclusivity of ships as a means for long-distance transport would not 

hold out forever. The use of roads, rail, and air provided new connections and 

routes for the movement of humans and animals as well as their microbes. For mi- 

crobes, the transportation revolution was really a connectivity revolution. These 

technologies created links that forever changed the nature of human infectious dis- 

eases, including, critically, how efficiently they spread. 

The use of roads of some sort or another is an ancient practice, far predating the 

use of water as a medium for transportation. Chimpanzees and bonobos both cre- 

ate and use forest trails to help them move through their territories. I learned this 

firsthand while studying wild chimpanzees in the Kibale Forest National Park in 

southwest Uganda. Richard Wrangham, the Harvard professor who introduced me 

to this work, used these trails to help observe chimpanzees.

Wrangham had done his doctoral work at the Gombe Stream site in Tanzania 

that Jane Goodall established. He’d critiqued some of the findings from Gombe 

because the chimpanzees there were habituated by provisioning—to get the wild 

chimpanzees comfortable with human researchers, the animals were fed large 

amounts of banana and sugarcane. Wrangham felt that provisioning changed 

some of the subtle chimpanzee behaviors, so when he started his own site in 

Kibale, he habituated the animals the hard way—by having his teams follow them 

until the apes effectively gave up and no longer ran away. He did this by essentially 

enhancing and extending the natural pathways that they moved along.³ 

The art of actual road building began in earnest around five to six thousand 

years ago when cultures throughout the Old World started using stone, logs, and 

later brick to enable the movement of people, animals, and cargo. The first modern 

roads followed in the late eighteenth and nineteenth centuries in France and the 

United Kingdom. These roads used multiple layers, drainage, and eventually ce- 

ment to make permanent structures permitting regular movement throughout the 

year. 

The rate at which modern roads have spread throughout the world has not been 

consistent, of course. Some regions in Europe and North America have roads 

reaching most human populations, while some regions where I work in central 

Africa have virtually no road access. Clearly, as roads enter into new regions, they 

bring both positive and negative effects. They are among the top priorities for many 

rural communities since they provide access to markets and health care, but from 

the perspective of global disease control, they are double-edged swords. 

HIV is among the most notable example of the impact that road proliferation 

has had on the movement of microbes. In a series of fascinating studies, the HIV 

geneticist Francine McCutchan, whose lab I worked in at Walter Reed Army Insti- 

tute of Research (WRAIR), and her colleagues at the Rakai and Mbeya sites in east 

Africa have examined the role that roads have played in the spread of HIV, demon- 

strating that proximity to roads increases a person’s risk of acquiring HIV. As peo- 

ple have more access to roads, they have a higher chance of getting infected be- 

cause roads spread people, and people spread HIV. Other than sex workers, the 

highest occupational risk for acquiring HIV in sub-Saharan Africa is being a truck 

driver. McCutchan and her colleagues have shown that the genetic complexity of 

HIV is greater among individuals who have increased access to roads. Roads

provide the mechanism for different types of HIV to encounter one another, in a 

single coinfected individual, and swap genetic information. But roads do more 

than just help established viruses spread. Roads and other forms of transport can 

also help to ignite pandemics. 

One of the most stubbornly lingering public misconceptions is that we don’t know 

how HIV originated. In fact, our understanding of the origins of HIV is more ad- 

vanced than our understanding of the origins of probably any other major human 

virus. As we saw in chapter 2, the pandemic form of HIV is a chimpanzee virus that 

crossed into humans.⁴ There is no debate within the scientific community on this 

point. The cumulative evidence with regard to how it originally entered into hu- 

mans is also increasingly unequivocal. It was almost certainly through contact with 

chimpanzee blood during the hunting and butchering of chimpanzees. We’ll delve 

further into this in chapter 9 when we discuss the work my colleagues and I have 

done with central African hunters. 

Perhaps the only lingering debate about HIV origins is how it originally spread 

from the first infected hunter and why it took so long for the medical community to 

discover it. The earliest historical HIV samples date from 1959 and 1960, twenty 

years before AIDS was even recognized as a disease. In an amazing piece of viral 

detective work, evolutionary virologist Michael Worobey and his colleagues man- 

aged to analyze a virus from a specimen of lymph node from a woman in 

Leopoldville, Congo (now Kinshasa, DRC). 

The lymph node had been embedded in wax for over forty-five years. By com- 

paring the genetic sequence of the virus they found in the specimen with other 

strains from humans and chimpanzees, they were able to attach rough dates for 

the first ancestor of the human virus. While the genetic techniques they used can- 

not pinpoint dates closer than a few decades, they concluded that the virus split 

from the lineage sometime around 1900 and certainly before 1930. They also con- 

cluded that by the time that the woman in Leopoldville became infected with HIV 

in 1959 there was already a significant amount of genetic diversity of HIV in Kin- 

shasa, suggesting that the epidemic had already established itself there. 

The fact that HIV goes back to 1959, let alone 1900, provides some serious 

challenges to the medical community. One of the central questions is this: if it was

in human populations in the early twentieth century and already constituted at least 

a localized epidemic in Kinshasa by 1959, why did it take us until 1980 to identify 

the epidemic? Another key question is what special conditions were present that 

permitted the virus to start taking off in the middle of the twentieth century? 

A number of changes occurred in francophone central Africa, the region where 

HIV-1 originated, leading up to the period in the 1950s when those first precious 

samples were taken. The anthropologist Jim Moore and his colleagues at the Univ- 

ersity of California, San Diego, put together some of the key events in a 2000 

paper, the majority of which focused on how easier means of travel influenced 

virus proliferation. In 1892 steamship service began from Kinshasa to Kisangani in 

the very heart of the central African forest. The steamship service connected pop- 

ulations that had been largely separated, creating the potential for viruses that 

previously might have gone extinct in local isolated populations to reach the grow- 

ing urban centers. In addition, the French initiated the construction of railroads, 

which, like shipping and road lines, connect populations. This produced another 

mechanism for viruses to spread from remote regions to urban centers, effectively 

providing a larger population size of hosts for a spreading virus. 

In addition to the connectivity provided by new steam, rail, and road lines, the 

construction of railroads and other large infrastructure projects led to cultural 

changes that also had an important impact. Large groups of men were conscripted, 

often forcefully, to build railroads. Moore and his colleagues note that the labor 

camps were populated mostly by men, a condition that dramatically favors trans- 

mission of sexually transmitted viruses like HIV. Together, the shipping and rail 

routes and the factors surrounding their construction must have played a role in 

the early transmission and spread of HIV. 

As dramatic as the road, rail, and shipping revolutions were for the transmission of 

microbes, an entirely new form of transport would add another layer of speed. On 

December 17, 1903, in Kitty Hawk, North Carolina, a site chosen for its regular 

breeze and soft sandy landing areas, the Wright Brothers made the first sustained, 

controlled, and powered flight. Some fifty years later the first commercial jet flew 

between London and Johannesburg. By the 1960s, the age of jet travel was here to 

stay.

Airplanes link populations in an immediate way, which allows the transmission 

of microbes to occur even more quickly. Microbes differ from each other in terms 

of their latent period, the period of time between when an individual is exposed and 

when they become infectious or capable of transmitting the agent to others.⁵ Al- 

most no microbes that we know of have latent periods of less than a day or so, but 

many have latent periods of a week or more. The immediacy of air travel means 

that even microbes with very short latent periods can spread effectively. In con- 

trast, if a person infected with an agent that had a very short latent period were to 

board a ship, unless the ship had hundreds of individuals the virus could infect, it 

would go extinct before the ship made land.

Commercial air flights alter in fundamental ways how epidemic disease spreads. 

In a fascinating paper from 2006, my colleagues John Brownstein and Clark 

Freifeld of Harvard, one of the new academic breed of digital epidemiologists, found 

creative ways to use existing data to show just how much impact air travel has on 

the spread of influenza. John and his colleagues analyzed seasonal influenza data 

from 1996 to 2005 and compared it with patterns of air travel. They found that the 

volume of domestic air travel predicts the rate of spread of influenza in the United 

States. Interestingly, the November travel peak around Thanksgiving appears to be 

of particular importance. International travel also plays a vital role. When the num- 

ber of international travelers is lower, the peak of the influenza season comes 

later—because when there are fewer travelers, it takes longer for the virus to 

spread. Perhaps most strikingly the researchers were able to see the impact of the 

terrorist attacks of September 2001 on influenza. The travel ban led to a delayed in- 

fluenza season. The striking effect was not seen in France, which did not enact the 

ban, providing an excellent control. 

  

During the past few centuries the ease of movement has increased dramatically 

throughout the world. The rail, road, sea, and air revolutions have all permitted hu- 

mans and animals to move more quickly and efficiently both within continents as 

well as between them. The transportation revolution has created interconnectivity 

unprecedented in the history of life on our planet. It is estimated that we now have 

over fifty thousand airports, twenty million miles of roads, seven hundred thou- 

sand miles of train tracks, and hundreds of thousands of ships and boats in the 

oceans at all times. 

The connectivity revolution we’ve experienced has fundamentally changed the 

ways that animal and human microbes move around our planet. It has radically in- 

creased the speed at which microbes can travel. It has brought populations to- 

gether, allowing agents that couldn’t previously sustain themselves with low popu- 

lation numbers to flourish. 

As we’ll see in chapter 8, it has also permitted completely novel diseases to

emerge and frightening animal viruses to extend their ranges. These technologies 

have created a single interconnected world—a giant microbial mixing vessel for 

infectious agents that previously stayed separate and stayed put. The new microbial 

mixing vessel that our planet has become has forever altered the way in which we’ll 

experience epidemics. It has truly helped usher us into the pandemic age.