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  During the next few years Hilleman and others performed a series of studies that were largely reassuring. Researchers found that although SV40 caused cancer when it was injected into hamsters, it didn’t cause cancer when it was fed to them. Sabin’s vaccine was swallowed, not injected. Researchers later found SV40 in the feces of children given Sabin’s vaccine, but none of those children developed antibodies to it. Apparently, SV40 just passed through the digestive tract without causing an infection. Researchers also found that although formaldehyde used in the making of Salk’s vaccine didn’t completely kill SV40, it did decrease infectivity at least ten thousandfold. The quantity of residual SV40 in Salk’s vaccine probably wasn’t enough to cause cancer. But at that point, no one was sure.

  Horrified that children had been injected with a potentially cancer-causing virus, researchers compared cancer rates in children who had received SV40-contaminated polio vaccines with cancer rates in unvaccinated children. Eight years after the tainted vaccines had been given, the cancer incidence was the same in both groups. The same was true fifteen and thirty years later. And it was true for children who had received SV40-contaminated vaccines in the United States, the United Kingdom, Germany, and Sweden. By the mid-1990s public health officials were confident that the inadvertent contamination of polio vaccines with SV40 didn’t cause cancer. Then an investigator at the National Cancer Institute in Bethesda, Maryland, found something that reignited the controversy.

  MICHELE CARBONE WAS INTERESTED IN FIGURING OUT WHAT CAUSED cancer. So he took cancer cells and studied their genes, hoping that they might provide a clue. Carbone studied unusual cancers of the chest (mesotheliomas), brain (ependymomas), and bone (osteosarcomas). Unlike leukemia, breast cancer, and prostate cancer, the cancers that Carbone studied are very rare. To his surprise, Carbone found one gene that kept turning up in each of the cancers—a gene that was also found in SV40. Carbone knew that SV40 caused cancer in hamsters and that the types of cancers found in hamsters were similar to those he found in people. The implication was clear: SV40-contaminated polio vaccines in the 1950s and early 1960s caused cancer. Carbone reasoned that the earlier studies had been falsely reassuring.

  Carbone’s findings stimulated another round of studies. This time, researchers looked specifically for Carbone’s unusual cancers. They studied hundreds of thousands—instead of just thousands—of people. But the results were the same. Again and again researchers found that people who had received vaccines inadvertently contaminated with SV40 were not at greater risk for cancer. Furthermore, they found that many people who had genetic fragments from SV40 in their cancer cells had never received contaminated polio vaccines. And they found that many adults had antibodies against SV40 in their blood even though they were born well before SV40-contaminated polio vaccines had been given.

  Keerti Shah, a professor at the Johns Hopkins School of Public Health, has been studying SV40 virus for more than forty years. When Carbone found genetic remnants of SV40 virus in lung cancers like mesothelioma, Shah also looked but couldn’t find any. “There was a big argument in 1998,” recalled Shah. “We could not find SV40 in mesotheliomas. Some labs would never find it, like ours. Some labs would always find it, like Carbone’s. There was a lot of controversy. People couldn’t figure out why this was happening. And there were many recriminations: ‘You don’t know how to do the assays. You’re messing it up.’ Then there was a study done by the National Cancer Institute and the Food and Drug Administration. Nine labs all tested mesotheliomas and also tested normal lungs as controls. In that study nobody found any SV40. And today all of the new [researchers] can’t find any evidence of SV40 in brain tumors or lymphomas or mesotheliomas.” Shah concluded that “SV40 never caused cancer in people.”

  Toward the end of his life, Hilleman was asked by Merck not to comment publicly about whether there was a link between SV40 and cancer, fearing that his comments might be misunderstood or used against him in pending litigation. But Hilleman was perfectly willing to talk privately. He had no doubt that the monkey virus that he had found contaminating polio vaccines in the mid-1950s didn’t cause cancer in people. “I advised [federal regulators] to pull the [polio] vaccine, but in retrospect I think they were right. Those vaccines never caused cancer. And disrupting the [polio vaccine] program would have cost thousands of lives.”

  The controversy surrounding SV40 contamination of polio vaccines is unlikely to die down soon, having recently triggered a series of lawsuits and the publication of a book, The Virus and the Vaccine: The True Story of a Cancer-Causing Monkey Virus, Contaminated Polio Vaccine, and the Millions of Americans Exposed by Debbie Bookchin and Jim Schumacher. Keerti Shah, who was interviewed extensively for the book, was troubled by its conclusion. “It was a well-researched book,” he said. “[The authors] did a great job digging up a lot of old materials. But they got the science wrong. And they saw conspiracies everywhere. There were no conspiracies.”

  Scared by the ordeal of SV40, researchers in the 1970s and 1980s made vaccines using cells from human fetuses instead of animals: vaccines that prevented rabies, chickenpox, and hepatitis A.

  TAD WIKTOR WANTED TO MAKE A RABIES VACCINE. LIKE STANLEY Plotkin, Wiktor would make his vaccine under the tutelage of Wistar’s director, Hilary Koprowski. Wiktor met Koprowski in Muguga, Kenya, while both were attending a conference on rabies organized by the World Health Organization. A tall, commanding man with the bearing of an army officer, Wiktor, like Koprowski, was Polish. Koprowski was instantly taken by Wiktor’s enthusiasm and intelligence and asked him to join the team at Wistar. Wiktor agreed and would stay until his death thirty years later.

  HILARY KOPROWSKI WAS IN AFRICA FOR ANOTHER REASON. DRIVEN to prevent the horror of polio—and locked in a competition with Albert Sabin—he wanted to test his live weakened polio vaccine in African children. Later, two journalists blamed Koprowski and his polio vaccine for the AIDS epidemic, calling him the father of AIDS. In 1992 Tom Curtis, an investigative reporter for Rolling Stone magazine, wrote an article titled “The Origins of AIDS: A Startling New Theory Attempts to Answer the Question ‘Was It an Act of God or an Act of Man?’” Several years later Edward Hooper, an unpaid stringer for the BBC in London, tried to prove Curtis’s allegation in his book The River: A Journey to the Source of HIV and AIDS. Curtis and Hooper used the following reasoning to explain why Koprowski’s polio vaccine was the source of AIDS: chimpanzees are occasionally infected with an HIV-like virus called simian immunodeficiency virus (SIV); the chimp cells that Koprowski used to make his vaccine were contaminated with SIV; SIV fed to African children mutated to HIV. As further proof, they noted that the AIDS epidemic started in central Africa at the same time and in the same place that Koprowski had inoculated children with his polio vaccine.

  But Curtis’s and Hooper’s theories, while fascinating, were flawed. First, the AIDS epidemic didn’t begin where Koprowski had performed his studies. Second, Koprowski didn’t use chimp cells to make his vaccine; he used monkey cells. (Chimps aren’t monkeys; they’re apes.) Finally, although some strains of SIV may have been precursors to HIV, mutation from one to the other would have taken decades, not years. The final proof that Koprowski’s polio vaccine didn’t contain either SIV or HIV came when researchers tested it using a sensitive assay called polymerase chain reaction (PCR), a technique that can detect very small quantities of viral DNA. Not surprisingly, researchers didn’t find SIV, HIV, or chimp cell DNA in Koprowski’s polio vaccine. In September 2000, Curtis’s and Hooper’s theories were finally and officially discredited on the stage of the Royal Society of London. Stanley Plotkin, who participated in the African polio vaccine trials, later commented on Edward Hooper’s search for the smoking gun behind the AIDS epidemic. “There was no gun, no shooter, no bullet, and no motive.”

  In May 2006 Beatrice Hahn and her colleagues at the University of Birmingham in Alabama proved that HIV was derived from SIV. Genetic analysis confirmed that SIV, which infected wild chimpanzees in C
ameroon, had crossed over to HIV in the early 1930s, twenty years before Koprowski began his polio vaccine trials in Africa. “The genetic similarity was striking,” she said. Presumably, a hunter in rural Cameroon was either bitten by a chimp or cut while butchering one.

  WIKTOR AND KOPROWSKI WANTED TO IMPROVE ON THE RABIES VACCINE that had been made before them. They knew that because Pasteur’s rabies vaccine was made from rabbit spinal cords, it occasionally caused weakness, paralysis, coma, and death. They also knew that researchers in the mid-1950s made a vaccine using duck embryos that was much less likely to cause these side effects. But because the duck vaccine still contained some cells from the duck’s brain and spinal cord—which contain myelin basic protein, an occasional cause of autoimmunity—it didn’t completely solve the problem. Also, the duck vaccine had to be given daily for about three weeks—twenty-three shots in the arms, legs, and abdomen. The procedure was so torturous that many people feared the vaccine more than they feared rabies. To make a better vaccine, Wiktor did what Stanley Plotkin had done. He visited Leonard Hayflick, his colleague at the Wistar Institute, and asked if he could have cells from the abortion that had been performed in Sweden in 1961. Wiktor knew that Hayflick’s cells didn’t contain SV40, were free of other contaminating viruses, and didn’t contain cells from the fetus’s brain and spinal cord—exactly what he needed. Within a few years Wiktor found that he could grow rabies virus in Hayflick’s cells and completely inactivate it with a chemical. Stanley Plotkin took Wiktor’s rabies vaccine and injected it into the arms of Koprowski and Wiktor, finding that it evoked high levels of rabies antibodies. Encouraged, the Wistar team took their vaccine to Iran, where wild rabid dogs roamed the streets, and injected it into people who had been severely bitten. The vaccine was 100 percent effective, worked after only a few injections, and was remarkably safe.

  Stanley Plotkin (left) inoculates Hilary Koprowski with experimental rabies vaccine as Tad Wiktor smiles for the camera, December 1971.

  Using Hayflick’s fetal cells, Tad Wiktor and Hilary Koprowski had solved the rabies vaccine problem, making a vaccine that is now given to ten million people every year. Unfortunately, many people who need the vaccine still don’t get it. Worldwide, rabies kills about fifty thousand people every year.

  THE NEXT VACCINE TO BE MADE FROM A HUMAN FETUS PREVENTED chickenpox. Prior to its invention, chickenpox virus infected four million people every year in the United States and a hundred million people worldwide. Although many people consider chickenpox to be a mild infection—a sort of rite of passage through childhood—it’s not. Chickenpox virus infects the brain, causing encephalitis; the liver, causing hepatitis; and the lungs, causing fatal pneumonia. (Patsy Mink, a congressional representative from Hawaii, died of chickenpox pneumonia in 2002.) Perhaps the most frightening problem—and the one that has attracted the most attention from the media—is that chickenpox causes a dramatic increase in diseases caused by Group A streptococci, the so-called flesh-eating bacteria. These bacteria invade the skin and muscles through broken chickenpox blisters. Before the chickenpox vaccine became available, chickenpox caused about ten thousand hospitalizations and a hundred deaths every year in the United States alone.

  When clinicians realized just how damaging chickenpox could be, they tried to make a vaccine to prevent it. Thomas Weller, who had used cells from a human abortion to perform his Nobel Prize–winning experiment with polio virus, took the first step. In 1951 Weller’s five-year-old son, Peter, got chickenpox. Weller broke open one of the blisters, collected the pus, and inoculated it onto cells from a variety of different species and organs. He discovered that human fetal cells worked best, a finding later confirmed by other investigators. “Every known human virus was found to grow in [human fetal cells],” recalled Hayflick. “That’s what made them so attractive for vaccines.”

  In the 1970s Michiaki Takahashi, a microbiologist working at Osaka University in Japan, took the next step. A slightly built, humble man, Takahashi made his vaccine in an unusual way. Like Weller, he took fluid from a blister of a child with chickenpox, a three-year-old boy whose family name was Oka. Then he passed the virus eleven times at low temperature through cells taken from an abortion in Japan, twelve times through fetal cells obtained from guinea pigs, two times through Hayflick’s cells, and five more times through cells from a fourteen-week-old male fetus aborted in the United Kingdom in 1966. The resultant vaccine virus is known as the Oka strain.

  Hilleman developed Takahashi’s vaccine and introduced it into the United States in 1995. By 2005, with almost all children receiving it, the number of infections and deaths from chickenpox declined 90 percent.

  THE LAST VACCINE TO BE MADE USING HAYFLICK’S CELLS PREVENTED hepatitis A virus. Before the vaccine, hepatitis A caused about two hundred thousand cases and a hundred deaths every year in the United States. In developing countries, where sewage and drinking water often mix, hepatitis A infects millions and kills thousands every year; almost everyone is infected. Hepatitis A virus also caused one of the largest single-source outbreaks of an infectious disease in United States history. It happened in western Pennsylvania.

  Jennifer Seavers was fourteen years old when she went out for Mexican food to celebrate a friend’s birthday. Although Jennifer didn’t like Mexican food, she didn’t want to miss the party. So in October 2003 she and a dozen girls from Ambridge High School sat down to plates of nachos, fajitas, and tacos at a Chi-Chi’s restaurant in Beaver, Pennsylvania, twenty-five miles northwest of Pittsburgh. Within a few weeks, one of Jennifer’s friends came down with fever, stomachaches, muscle pain, weakness, nausea, and vomiting. Her urine turned dark brown, her skin turned yellow, and she couldn’t breathe without feeling as if she was being stabbed just below her ribs. Frantic, the girl’s parents took her to the doctor, whose blood test revealed the diagnosis: hepatitis A.

  Jennifer knew that she had dodged a bullet. “I feel really lucky that I didn’t get sick,” she said. “But I know a lot of people who did.” Jennifer’s friend was one of many. The first case of hepatitis occurred on October 2, 2003. During the next few weeks, several more people in that area got sick. By November 3, local health officials confirmed that there was an outbreak of hepatitis and asked Chi-Chi’s to shut its doors. Because the time from exposure to the virus to the appearance of first symptoms can be as long as seven weeks, everyone who had eaten at the restaurant from September to November was at risk; Chi-Chi’s had served eleven thousand meals during that time. By November 5, the number of people infected had risen to eighty-four; by November 6, to a hundred and thirty; and by November 7, to two hundred. On November 7, Jeffrey Cook, an auto-body restorer from Aliquippa, Pennsylvania, died following a liver transplant in a desperate attempt to save his life.

  Health officials were sure that the outbreak was caused by a restaurant employee, and during their investigations they found several employees with hepatitis. But all had been infected at the same time as their customers, not before. The timing wasn’t right. The virus was coming from somewhere else. By November 11, the number of people infected had risen to three hundred, and two more people were in critical condition. By November 12, after forty more people became ill, investigators finally closed in on a likely source. Earlier that year, public health officials had interviewed thousands of people during outbreaks of hepatitis A in Georgia, Tennessee, and North Carolina. They had asked people who had and hadn’t gotten sick what they had eaten. Then they had carefully checked the ingredients of each of those foods. One item kept appearing on the list of hepatitis A victims: green onions (scallions). Investigators found that restaurants had imported their green onions from Mexico, a country with a high rate of hepatitis A infection. Richard Quartarone, a spokesman for the Georgia State Health Department, said, “Because they’re multilayered, green onions are very difficult to clean. The only way to be 100 percent sure that you’ve killed the hepatitis in the green onions is to cook them. But they’re often used as a garnish, so you don’t c
ook them.” Chi-Chi’s, which had imported its green onions from Mexico, immediately pulled them from the menus of their ninety-nine other restaurants from Minnesota to the mid-Atlantic. But it was too late.

  By November 13, the number of cases had risen to four hundred, and the outbreak claimed its second victim, Dineen Wieczorek, a customer service representative for Ikea. She had eaten at Chi-Chi’s on October 6 to celebrate her wedding anniversary. Her daughter, Darleen Tronzo, recalled, “One meal. One meal, that’s all it took. And people eat out every day. I eat out every day. You never think something like this could come of it.” By November 14 the number of cases had risen to five hundred, and the outbreak claimed its third victim, John Spratt, an employee at a payroll processing company. Spratt had eaten at Chi-Chi’s with his daughter. They had both ordered the chicken fajitas. But Spratt, not his daughter, had chosen to eat the condiments that came with the meal—a choice that killed him.