Oh, you may be sure that Columbus was happy not when he had discovered America, but when he was discovering it.
—Fyodor Dostoevsky, The Idiot
EARLY DURING HIS studies at the University of Pennsylvania, Hayflick enrolled in an introductory course in what was then called bacteriology.
On his first day in the lab, a technician walked in carrying something that changed Hayflick’s life. It was a tray of test tubes containing a nutritious, gelatin-like substance called agar, which was a dull chicken-soup color. The test tubes had been tilted so that the agar, initially poured into the tubes in liquid form, solidified on a slant, maximizing the surface area available for bacteria to grow on. The technician had then used a fine needle to inoculate each tube with a different kind of bacterium, dragging the needle in a wave pattern along the yellow brown agar to “streak” it. What the young Hayflick saw was the resulting bacterial growth. The slants were streaked with a rainbow of colors, from yellow to purple, green, white, and pink.
Hayflick was blown away. He decided on the spot to major in bacteriology. (The discipline would soon be relabeled “microbiology,” in order to encompass viruses as well as bacteria.)
Hayflick’s love affair with microbes began at the dawn of a golden age for the study of viruses. The study of bacteria—bigger organisms that can survive independently outside of cells—was older. Scientists had been growing and examining bacteria in lab dishes since the late 1870s, when a German microbiologist named Robert Koch developed practical methods of growing pure cultures of bacteria in the lab. Koch also decisively laid out the steps that biologists needed to take to prove that a given bacterium was causing a particular disease. Biologists began to link specific bacteria with diseases, to understand how they were transmitted, to track outbreaks, and to launch the first therapeutic salvos against bacterial banes like diphtheria and syphilis.
The ease with which bacteria could be grown in lab dishes was vital not only for studying them but also for the discovery and testing of the antibiotics that were new miracles in the late 1940s: drugs like sulfa and streptomycin. The most famous among these was discovered when a short, slight Scotsman named Alexander Fleming noticed something strange on an agar plate on which he was growing Staphylococcus bacteria in his lab at St. Mary’s Hospital in London. A mold had accidentally taken root on the petri dish, and the bacteria, which were thriving elsewhere on the dish, wouldn’t grow anywhere near the mold. That moldy invader, it emerged, made a substance that Fleming named penicillin.
Virology was a slightly younger and decidedly less well-equipped science. Viruses had been known to exist since the early 1890s, when a young Russian scientist named Dmitry Ivanovsky took sap from the yellowed, stunted leaves of plants with tobacco mosaic disease and passed it through a filter containing pores too tiny for bacteria to slip through. (Bacteria are enormous compared with viruses. Consider that HIV, a typical-sized virus, is a mere golf ball compared with the soccer ball that is Streptococcus pyogenes, the diminutive bacterium that causes strep throat today but regularly killed kids when Hayflick was a child.)
The filtered fluid from the diseased tobacco leaves was able to infect other, healthy tobacco plants.1 Soon a Dutch botanist, Martinus Beijerinck, who had done similar experiments, demonstrated that whatever was causing the tobacco-plant disease could reproduce itself but needed living cells in which to do so.2 He became convinced that the disease-causing entity was a liquid, and he christened it with a Latin name, “virus,” which means “slimy fluid.”
The same year, 1898, a pair of German scientists, Friedrich Loeffler and Paul Frosch, found that they were able to pass along a devastating animal affliction, foot-and-mouth disease, by taking fluid from the sores of infected calves, filtering it, and using the filtrate to infect other animals—the first proof of animal infection by these mysterious new entities, which scientists began calling “filterable agents.”3 (It would be some time before the term “virus” came into common use.) The German duo also surmised, correctly, that the infectious agent wasn’t a liquid but a particle so small that the filter did not capture it.4 The pair also developed what was probably the first killed-virus vaccine, taking fluid from the sores of infected animals, heating it to destroy its infectivity, and injecting it into nonimmune cows and sheep, the overwhelming majority of which were then protected from the disease.5
In the next half century some dozen viruses that cause human diseases were identified, including the viruses that cause yellow fever, rabies, polio, and influenza. Dozens of animal and plant viruses were also found. In 1927, Thomas Rivers, an eminent American microbiologist, defined viruses as “obligate parasites,” meaning that they could reproduce only by invading living cells.6 In 1928, the year of Hayflick’s birth, Rivers published Filterable Viruses, a collection of essays of which he was editor, describing the roughly sixty-five viruses that had been identified to that date.7
But identifying viruses was hardly tantamount to understanding them, never mind fighting them. And the fact was, for the first half of the twentieth century, scientists investigating human-infecting viruses were hobbled by the difficulty of getting at them. That was because, unlike bacteria, which live happily and independently in lab dishes as long as they’re nourished with nutritious substances like agar, viruses need living cells in order to survive.
At its most basic, a virus consists of a circular or linear thread of genetic material—DNA or its chemical cousin, RNA—and a protective protein coat. It reproduces itself by invading a cell and forcing the host cell’s machinery to make tens, hundreds, or thousands of copies of the virus in one huge burst, sometimes in the space of minutes. These new viruses—each virus is called a virus “particle”—then bud or burst out of the cell and proceed to invade other cells. (Some viruses can also move directly from cell to cell.)
Despite their formidable talent for hijacking, viruses are helpless on their own. They are not independent organisms that propel themselves around, eat, digest, excrete waste, or have sex. Their sole business is to invade living cells so they can reproduce. So while they can survive on nonliving objects and surfaces for hours, days, weeks, and sometimes months, they are merely inert chemicals when they are sitting in, say, a test tube. It is “only in the interior of a living cell [that a virus’s] hidden forces are liberated,” the Swedish virologist Sven Gard—who will play a role in this story—observed as he presented the Nobel Prize in 1954.
But how then to study human viruses? Sometimes scientists relied on human heroism. Walter Reed, the famous U.S. Army physician who proved that yellow fever was caused by a mosquito-borne virus, did so by enlisting volunteers who were willing to be bitten by mosquitoes that had recently fed on yellow fever–infected patients. One of Reed’s medical colleagues, Jesse Lazear, was infected and died in that decisive experiment in 1900.
Sometimes virologists could use living animals to study human diseases, like the group of British investigators who, during an outbreak of influenza in 1932, noticed that some of their furry laboratory ferrets, being used for other purposes, were sneezing. They had caught human influenza from the sick scientists. (Later the reverse also happened.) From then on, the group studied influenza by using a pipette to drop throat garglings from infected people onto ferrets’ noses. When the disease was at its height, they would sacrifice the ferrets and study their tissues. But observing the damage to animals—rather than observing the virus itself—was hardly satisfactory. And yet viruses were too small to be seen with the light microscopes that were then available. Besides which, many human viruses did not infect other animals.
In some limited cases scientists succeeded in growing human viruses in lab dishes, using a little-understood art called tissue culture. Tissue culture today is more commonly called cell culture. It means growing living cells in the laboratory, outside of the animals or plants that they came from. (It will play a central role in this book.) Ross Harrison, a brilliant, driven biologist then at Johns Hopkins University, is credited with launching tissue culture in 1907, by growing bits of frog embryo brain in the lab. By nourishing the frog brain cells with fluid from the frogs’ lymph glands, he kept the cells alive for weeks.
In the following three decades virologists would manage, with difficulty, to grow several viruses in tissue culture—for instance, in fresh, minced hen’s kidney bathed with blood serum (the liquid, noncellular part of blood). But their successes were sporadic and inconsistent. Soon the viruses would die out in their dishes. Over these decades the only practical accomplishment to come from the use of tissue culture in virology was this: in the 1930s Max Theiler, a South African–born virologist at the Rockefeller Institute in New York City, weakened the human yellow fever virus by growing it in minced chicken embryos, developing the yellow fever vaccine that is still used today.
This achievement was the exception when it came to viruses—in stark contrast to the strides being made against their bacterial counterparts. By the middle of the twentieth century, bacterial diseases were being beaten back by vaccines against once-common killers like diphtheria, tuberculosis, and whooping cough—and by antibiotics. These new wonder drugs shut down bacteria, but they didn’t target viruses, which, because of the way they co-opt the native machinery of host cells, are harder to take aim at without producing off-target side effects. The first antiviral drugs wouldn’t begin to be developed until the 1960s. And so, as Hayflick stood, transfixed, before those rainbow streaks in a bacteriology lab at the University of Pennsylvania, viral illnesses like measles, rubella, and hepatitis remained stubborn, dangerous banes—with polio the most visible and frightening among them.
The discovery that changed everything for virus hunters happened in 1948, just as Hayflick returned to Penn from the army. In the spring of that year, an unassuming, middle-aged scientist was laboring in a small lab at the Boston Children’s Hospital. John Enders came from a wealthy New England banking family. He enjoyed the poetry of T. S. Eliot, favored old tweed jackets, and had flown rickety biplanes as a flight instructor during World War I. He had failed as a real estate agent before developing a passion for biology and earning a PhD at Harvard. Enders and his younger colleague Thomas Weller, a pediatrician from a family of physicians, had been trying to improve tissue-culture techniques for a decade—interrupted by World War II, when Weller had served in the Army Medical Corps. They had lately been joined by a third virus hunter, Frederick Robbins, an infectious-disease physician who had served in the army in North Africa and Italy, winning a Bronze Star. The trio was about to break open the world of virology, allowing scientists to grow a plethora of viruses in many tissues in lab dishes. With the application of their techniques, viruses would no longer die out in their dishes but would continue to multiply, allowing for study—and vaccine making.
Apart from sheer, dogged hard work, there were three key developments that led to the Enders team’s success. First, tissue culturists were figuring out, slowly, how to improve the nourishing solutions that they used to keep cells alive in lab dishes. Second, the Boston scientists put to good use a roller-tube system invented fifteen years earlier. Something like a Ferris wheel, it slowly rotated cells in test tubes, lying on their sides, eight to ten times every hour. This allowed the cells to be first washed in nutrient fluid, then exposed to air, in an attempt to mimic the conditions in the human body with its ceaseless flow of oxygenated blood to and waste removal from cells. Third, and crucially, as the 1940s progressed, Enders also took advantage of a new tool: antibiotics, which he began religiously applying to his test-tube cultures. He hoped, correctly as it turned out, that they would eliminate contaminating bacteria but leave viruses thriving.
One day in March 1948, Enders made a seemingly off-the-cuff suggestion to his junior partners. It involved polio. Poliovirus had resisted attempts to corral it in culture dishes, with this exception: In the mid-1930s a brilliant, ambitious young scientist named Albert Sabin, working with his senior colleague Peter Olitsky at the Rockefeller Institute in New York City, managed to grow polio in nerve cells from the brains and spinal cords of two aborted human fetuses.8 (The spinal cord, like the brain, is composed mainly of nerve cells, called neurons.) The duo had obtained the three- to four-month-old fetuses from a physician colleague at Bellevue Hospital, dissected their organs, and stored them in a lab refrigerator. Their experiment was groundbreaking not only for what it reported about polio but also for being one of the first published studies to use human fetal tissue in the lab.
In the 1930s abortion was a crime in every U.S. state in most circumstances.9 And indeed, most of the estimated 800,000 abortions that were conducted annually during the economically stressed 1930s were illegal.10 The exceptions were known as therapeutic abortions; they reflected an unwritten understanding between legal authorities and physicians that the latter would be allowed to conduct abortions they deemed medically necessary or advisable. Therapeutic abortions were conducted at abortion clinics or medical offices by licensed physicians. But this was not an age of placard-carrying demonstrators outside clinics. These were procedures done out of public view. In the same way, fetal tissue research was conducted out of sight of the public and at the will of researchers.
No one had tried growing polio in human cells. Since polio attacked the nervous system to cause paralysis, Sabin and Olitsky surmised that it would grow in nerve cells. And so they minced the fetal brains and spinal cords and placed the resulting bits of tissue in wide-bottom flasks. Then they added poliovirus from the ground-up spinal cords of infected monkeys. The virus multiplied in the fetal nerve cells—as proven by the fact that when the scientists took fluid from the cultures bathing the fetal cells and injected it into the brains of monkeys, the animals became paralyzed.
Ironically, the paper that Olitsky and Sabin published actually slowed the hunt for a polio vaccine. Why? Because the Rockefeller duo also reported “complete lack of growth” of polio in cultures of other organs from the fetuses, including kidneys and lungs. The “special affinity of the virus for nervous tissue” disqualified the virus for vaccine-making purposes, because viral vaccines contain tiny bits of the cells in which they are made, and nerve cells, when injected into people, were known to occasionally cause a dangerous and sometimes fatal allergic reaction: an inflammation of the brain and spinal cord called encephalomyelitis.
And so very little progress against polio was made until twelve years later, at the Enders lab in Boston. Early in 1948 Enders, Weller, and Robbins were deep into studies trying to grow mumps, measles, influenza, and chicken pox viruses in culture. Enders had called on a physician colleague at the Boston Lying-In Hospital, to provide aborted embryos and fetuses.
He received several from abortions conducted at 2.5 to 4.5 months of pregnancy, as well as a stillborn infant delivered at seven months of pregnancy. Weller minced the skin, muscle, and connective tissue from the fetal arms and legs and distributed it in flasks. The plan was to inoculate the flasks with chicken pox virus from the throat of a sick child. But as they were preparing to do so, Enders casually suggested that Weller and Robbins also inoculate an equal number of flasks with poliovirus from infected mouse brains that were also on hand in the lab. The experiment was timely because virologists, Enders among them, were beginning to doubt the handed-down wisdom that polio would only grow in nervous tissue. For one thing, the virus was being found in quantity in the feces of polio-infected people. Enders was skeptical that a virus that resided strictly in nerve cells could turn up in such profusion in the intestinal tract.
The chicken pox cultures grew nothing. But the poliovirus grew spectacularly, and when the scientists injected fluid from the polio flasks into the brains of mice and monkeys, they became paralyzed. The Enders lab had made an enormous leap. It turned out that Sabin and Olitsky had failed in their experiments thirteen years earlier because they were using a particular strain of polio that would grow only in nerve tissue. Other strains were far less choosy.
The momentous discovery was described in a short article buried in the back of the journal Science in January 1949.11 When polio virologists saw the report, “it was like hearing a cannon go off,” Rivers, the dean of U.S. microbiologists, recalled later.12 Not only had they cornered polio, but Enders and his colleagues had delivered the methods that would allow scientists to grow, without limit, many kinds of viruses in many kinds of tissues.
The Enders lab’s breakthrough soon made possible the isolation of scores of new viruses—including viruses that infected only humans and grew only in human cells. And scientists could now readily study the effects of those viruses on cells in the lab, rather than in living animals. Of most immediate import for the public, the discovery also made possible within a few years the industrial-scale growth of poliovirus in nonnervous tissue in lab dishes, allowing the development of polio vaccines.
In 1954 the Nobel Committee in Sweden honored Enders, Weller, and Robbins with that year’s prize in physiology or medicine. Their discovery had thrown open the doors to virology. It also made tissue culture a vital part of coming advances. He didn’t know it yet, but Leonard Hayflick would land squarely in the middle of the new push forward.
Hayflick graduated from the University of Pennsylvania in the spring of 1951 with a BA in arts and sciences and a double major in microbiology and chemistry. He went to work as a research assistant at a drug company called Sharp & Dohme in Glenolden, a Philadelphia suburb. There he helped make a product to dissolve clotted blood and pus in infected surgical wounds. Soon Sharp & Dohme merged with the big drug company Merck, which had built a brand-new research facility twenty-seven miles northwest of Philadelphia in West Point.
Sharp & Dohme had been something of a scientific backwater. At the state-of-the-art Merck labs Hayflick was exposed to new and exciting things. He began to learn about viruses like bacteriophages, which attack and invade bacteria. He saw firsthand the excitement of the hunt for new antibiotics at a time when the drugs were transforming medical practice. He also saw for the first time highly educated commercial scientists in action. A revolutionary ambition began to take hold in Hayflick’s head and heart. He had never let himself consider getting a PhD.13, 14
Hayflick applied and was admitted to the doctoral program in medical microbiology at the University of Pennsylvania. He enrolled in the fall of 1952. He had saved enough money to pay the tuition and to get by if he continued to live at home. After his first year in the program, he would receive university scholarships and a fellowship that supported him through the rest of his PhD studies.
Just before Hayflick left Merck, Sharp & Dohme in June 1952, he met a talented young artist who worked preparing slides for scientists at the West Point facility. The pair discovered that they both planned to travel in Europe that summer and that their separate itineraries had them crossing paths in Paris.
Ruth Louise Heckler was a slim, self-assured twenty-six-year-old with a broad smile and a quiet demeanor that comported well with Hayflick’s own. She was from a churchgoing Pennsylvania Dutch family in Lansdale, a railroad town not far north of Philadelphia, where her father worked as an accountant for the Lehigh Coal & Navigation Company. She had studied life drawing and book illustration at the Philadelphia Museum School of Industrial Art before coming to Merck.
Heckler was drawn to Hayflick’s mind—his ability to analyze problems clearly and quickly.15 He was drawn to her quiet self-assurance, her intelligence, and her questioning of religious authority; she had rejected the Lutheranism of her childhood and begun attending Quaker meetings. He also found her beautiful: one day as they walked in Paris, he put his arm around her waist. On October 2, 1955, with Hayflick in the final year of his PhD, the couple were married in a simple, intimate service at the 150-year-old Arch Street Friends Meeting House in Philadelphia. There was a dry reception in the hall next door, and then the newlyweds walked to a nearby Reform synagogue on Broad Street, where a rabbi blessed their union.
For his PhD thesis Hayflick studied a mysterious group of microbes then called pleuropneumonia-like organisms, or PPLOs. (They have long since been renamed Mycoplasma.) These microbes had been known for two centuries to cause a highly contagious pneumonia in cows in Europe, but they were still poorly understood. Too large to be viruses and yet smaller than bacteria, they defied categorization and their links to other animal and human diseases were murky.
Hayflick was intrigued by PPLOs and grew to be equally taken with the newly exciting art of tissue culture. His graduate mentor—assistant professor Warren Stinebring, a soft-spoken, stocky former college football player—was full of energy about a course he had just taken in tissue culture, one of the first of its kind. He wanted to train Hayflick. Hayflick didn’t want to be distracted from his PPLOs but agreed to a compromise: for his thesis project he would grow PPLOs in tissue culture. Hayflick was working in primitive conditions by today’s standards. He grew his PPLOs in a chicken incubator bought for less than $40 from a Sears Roebuck catalog.
Early in his graduate studies Hayflick began to spend time at a nearby institute that would have a huge and lasting impact on his professional life. He recalls being asked to investigate an outbreak of a middle-ear infection in a famous colony of pink-eyed, snow-white research rats. The albino rats were known to all as Wistar rats, because they were developed and resided at the Wistar Institute of Anatomy and Biology. They were an important laboratory tool, but the infections had upset their balance and left them spinning in purposeless circles. PPLOs were possibly the culprit.
The Wistar, as people called it, was a gracious, V-shaped, three-story building of light brown brick located on prime real estate in the heart of the University of Pennsylvania campus. A stone’s throw from the iconic statue of Benjamin Franklin on Penn’s main quad, the institute was the oldest freestanding biological research organization in the country. It was completely independent of Penn, having been founded in 1892 by a wealthy, eminent Philadelphia family. The Wistars included Caspar Wistar, an eighteenth-and-nineteenth-century physician and anatomist who wrote the first U.S. textbook of anatomy and in the process amassed and preserved a huge number of anatomical specimens. Caspar Wistar’s great-nephew, Isaac Wistar, a Civil War brigadier general and a prominent Philadelphia attorney, established and endowed the institute to preserve and display his great-uncle’s impressive collection.16
The brain of Isaac Wistar—at his request—was preserved in a big glass jar in the basement of the institute, along with his right arm, shriveled from a Civil War wound. His ashes were, and still are, in an urn that overlooks the atrium. (If officials of the newly founded institute had had their way in the 1890s, they would also have displayed the gray matter of the psychopath Henry Holmes. The Wistar tried without success to obtain his brain for study after the hanging of the serial killer who haunted the 1893 Chicago World’s Fair.)17
In the mid-1950s the Wistar Institute was a strange mix of faded elegance and creepiness. It boasted terra-cotta detail on its facade, an airy atrium surrounding a broad wrought-iron staircase, and a public museum on the first floor that was the stuff of horror movies. There were reptiles from Borneo and the bladder stones of Chief Justice John Marshall (removed without benefit of anesthesia). There were human bones gathered on the field after the 1815 Battle of Waterloo and a wide selection of human skulls used to teach medical and dental students. There were seven wax-injected human hearts. There was an intact skeleton of what had been Siamese twins. And floating in formalin, in patented display cases, there was the largest collection of embryos and fetuses in the country, many of them with abnormalities like clubfoot and cleft palate.18
But despite the crowds of school children who regularly trooped through the locally famous museum, the Wistar Institute in the mid-1950s was slowly dying from decades of neglect. Its wiring and plumbing were failing. Its senior staff comprised exactly three scientists, two of them in their eighties. And since 1940 its inertia-ridden board of managers had left the institute to be run by a less-than-ideal acting director. Perceiving the lack of leadership, junior scientists came and went very quickly.19
This acting director—a short, quick, domineering man named Edmond Farris—was a middling PhD scientist and not a physician at all, but he had made himself indispensable to certain Philadelphia couples by launching an infertility clinic that he ran out of the Wistar, fueled by the sperm donations of University of Pennsylvania students.20 In addition to artificial insemination, Farris’s services included microscopic examination of the male partner’s sperm for deficiencies. He also ran pregnancy tests by injecting a woman’s urine into a prepubescent female rat from the Wistar colony. If the rat went into heat despite its immaturity, that indicated the presence in the woman’s urine of a female hormone made only during pregnancy. (Early in 1956, two decades before home pregnancy tests were available, Hayflick and his wife took advantage of the in-house services. The couple’s first child, Joel, arrived later that year.)
The lab that Hayflick chose for pursuing his rat assignment, on the otherwise-empty second floor, had antique Bunsen burners and wrought-iron filigree. Hanging outside the door, suspended from the high ceiling of the atrium, was the skeleton of a seventy-foot finback whale sold to the institute in 1897 by the renowned paleontologist Edward Drinker Cope.21 Far from putting him off, the eerie, empty environs fascinated Hayflick, who enjoyed working alone in the lab on the second floor or thumbing through the collection of ancient scientific books in the eighteen-thousand-volume library. Occasionally he encountered one of Edmond Farris’s happy customers climbing the wrought-iron staircase with a new baby in her arms.22
In the spring of 1956 Hayflick received his PhD. He had, indeed, shown that PPLOs could be grown in tissue culture.23 (He also confirmed that a PPLO had sickened the Wistar rats.) He was no longer an uncertain undergraduate. And he had new, outside affirmation of his abilities. He had won a postdoctoral fellowship endowed by A. C. McLauglin, a Colorado oil tycoon. It would take him to Galveston, Texas, to the lab of Charles Pomerat, the man who was arguably the best tissue culturist in the world. The fellowship paid a considerable sum in Hayflick’s world: $5,500, tax free. He and Ruth moved to Galveston in August 1956.
The charismatic Pomerat, a bald, portly man who wore a butcher’s apron and favored white duck trousers, ran a big lab in the basement of the psychiatry building at the University of Texas Medical Branch in Galveston. It was a place that hummed with activity, its tone set by its chatty leader, who was not only a pioneer cell culturist but also an outstanding chef and an accomplished artist. Pomerat had pioneered a new tool: time-lapse microscopic photography of cells in action, with exposures made every thirty or forty seconds and rendered on reel-to-reel films.
At any given time Pomerat would have several cameras peering down long tubes running down to the microscopes, where they focused on cells in a minuscule chamber. The lab was full of a constant clicking of shutters and attendant flashes of light emanating from the tops of the microscopes.
Hayflick used the cameras to study adenoviruses, a class of viruses that had recently been discovered in human tonsils and in the adenoid tissue after which they were named: glandular tissue in the back of the throat. He was able to observe the effects, hour by hour, as adenoviruses destroyed cells. Holes would appear in the cells’ cytoplasm; the cells would sprout abnormal, armlike extensions. Finally, they would break apart. Hayflick did not make any grand discoveries in Galveston, nor could he publish in journals the reel-to-reel films he produced. But he became increasingly expert in cell culture, and he rubbed shoulders with and learned from first-rate scientists like Morris Pollard, an eminent virologist. Hayflick also met a colleague of his own age who would play an important part in his career. Paul Moorhead was a blue-eyed Arkansan with adamantly liberal politics and a passion for chromosomes—the long, stringy bundles of DNA that are housed in a cell’s nucleus and contain its genetic material.
Ruth gave birth to Joel in November 1956. The Hayflicks’ second child, Deborah, was born thirteen months later, while Hayflick was still in the Pomerat lab. Once or twice a night he would wake, give a bottle to a baby or two, then drive to the lab to adjust the microscope, which would inevitably slide out of focus after a few hours.
Early in his second year in Galveston, Hayflick began looking toward his next step. He heard that the Wistar Institute, after nearly two decades under an acting director, had finally hired a permanent chief. He was a polio vaccine pioneer named Hilary Koprowski, and he was looking for a cell culturist. Hayflick applied and received an offer. It was “scut work,” providing cell cultures to Wistar scientists, and not the pure research position he would have preferred.24 Still, it could lead to bigger things, and he was sure he could squeeze in his own research on the side. It would also take him and Ruth back to their families and friends in Philadelphia. He began work at the Wistar, his old stomping ground, in April 1958, one month shy of his thirtieth birthday.