Vaccinated (12 page)

It's unlikely that vaccine makers are going to remake routine children's vaccines—such as those for rubella, hepatitis A, and chickenpox—at great cost for no financial benefit. And inflammatory, incorrect statements regarding vaccines in current use don't help. “The widespread use of these vaccines makes it very likely [that] additional cell lines will be created from other aborted babies,” says Vinnedge. “As opposed to the Nazi Holocaust, the abortion Holocaust is ongoing.” But the truth is that no new abortions are performed to make any of these vaccines. The cells frozen from the abortion performed in 1961, periodically thawed and grown in laboratory flasks, constitute all that is necessary to make them for generations.

 

L
EONARD
H
AYFLICK, THE MAN WHO HAD GIVEN FETAL CELLS TO
P
LOTKIN
, Wiktor, Hilleman, and Takahashi to make their vaccines, became a pariah. In 1968 Hayflick left the Wistar Institute to become a professor of medical microbiology at Stanford University School of Medicine. He took his fetal cells with him. Hayflick had already set up a company called Cell Associates, with him and his wife as sole proprietors, which sold fetal cells to hundreds of researchers throughout the world. Hayflick charged researchers his costs for preparing and shipping the cells, never profiting from the sales; the total proceeds were only about $15,000. But some saw Hayflick as profiting from his work. “In those days, in that environment,” recalled a Wistar co-worker, “when you did research with government support, it was in the public domain. When it came out that Len was selling these cells, a lot of people were appalled.”

Well funded by the NIH, in the midst of making important discoveries about how and why we age, and well respected by many of his fellow scientists, Hayflick was at the top of his game. But two years later Leonard Hayflick was standing in an unemployment line in Palo Alto.

On January 30, 1976, James W. Schriver, a management accountant at the NIH, filed a report claiming that Hayflick was selling something that wasn't his to sell. Schriver claimed that because Hayflick's research was funded by the NIH, money made from the sale of fetal cells should be paid to NIH, not Hayflick. Stanford's School of Medicine, alarmed by the growing scandal, concluded that Hayflick had acted unethically. On February 27, 1976, Leonard Hayflick resigned. “In 1975 I took the first initiative and asked the director of NIH to make a definitive determination about [who owned my fetal] cells,” recalled Hayflick. “Instead of sending a lawyer or a scientist, who might understand my claim, they sent an accountant, who went to Clayton Rich [Stanford's dean] and said ‘Do you know that you have a thief in the microbiology department?' [The dean was] advised by the bookkeeper that his cooperation was expected because 90 percent of [Stanford's] budget came from NIH. Stanford University called the campus police and asked them to call the district attorney. Public servants from the NIH [then] entered my laboratory, confiscated [my fetal cells], and claimed them for themselves. The NIH maintained that it was perfectly fair for commercial organizations, the Russians, and themselves to sell [my fetal cells] for tens of millions of dollars, but they viewed as theft the inventor or his institution profiting.” In the eyes of his fellow scientists, Hayflick was ruined. “I went from full professor at Stanford to the unemployment line in one week,” he recalled. “My wife and I lived on $104 a week for the next year.” Plotkin remembered the controversy: “I think that in the really classical Greek sense it was a tragedy because here was a man who at the height of his powers brought about his own downfall.”

Hayflick sued the federal government, which in turn countersued. “I felt, and I think I was justified in feeling, that these cells were like my children,” he said. Hilleman, who was asked to testify against Hayflick, recalled, “I was asked to be a principal witness against him. And I said that if there was an attempt to convict him, I would make a campaign on my part that two top-level government officials would spend time in jail with him. He should have been celebrated as a scientific hero instead of being persecuted.” In September 1982, after six years of wrangling, the case was settled out of court—in Hayflick's favor. Hayflick was awarded the principal plus interest of the $15,000 that had been held in escrow, and the government allowed him to keep his cells. Hayflick never kept the settlement award, using it to pay his lawyers. Colleagues rallied to his support. A letter signed by eighty-five scientists was published in the journal
Science
: “This happy outcome of Dr. Hayflick's courageous, sometimes lonely, emotionally damaging, and professionally destructive ordeal provides several important object lessons for the future. In light of the settlement terms and other government actions, few will disagree that the original allegation against him was entirely unjustified.” Hayflick's battle changed the law. Now scientists receiving federal money can own and sell their discoveries. This single ruling allowed for the boom in private-sector biotechnology in the 1980s and 1990s. “I was a pioneer,” recalled Hayflick. “And it's the pioneers that have the arrows in their backs.”

 

A
LTHOUGH THE USE OF FETAL CELLS TO MAKE VACCINES REMAINS CONTROVERSIAL
for some, the vaccines made from them are safe. Fetal cells allowed Hilleman and others to avoid contaminating viruses like chicken leukemia virus and SV40. But Maurice Hilleman was about to use a material to make his next vaccine that few thought was safe, even after the vaccine had been licensed and sold: human blood. Hilleman obtained blood from drug abusers and homosexual men living in New York City in the late 1970s, when HIV first entered the United States. It was arguably the most dangerous starting material ever used to make a medical product.

I
n 1984 researchers at the CDC published a paper titled “Cluster of Cases of the Acquired Immune Deficiency Syndrome (AIDS): Patients Linked by Sexual Contact.” AIDS, a syndrome that included unusual infections and cancers, was sweeping across the country. Thousands had been infected.

Victims of AIDS died of many different diseases. For example, they died of pneumonia. Before AIDS entered the United States, pneumonia caused by pneumococcal bacteria killed tens of thousands of people every year. But AIDS patients were different; they were killed by
Pneumocystis
, an organism previously found to cause pneumonia only in cancer patients. They also died of meningitis—but again, not from typical bacteria, such as meningococci, but from unusual fungi such as
Cryptococcus
. Or they died of Kaposi's sarcoma, a previously rare form of cancer that caused hideous dark purple spots under the skin.

The CDC researchers found several groups of people at high risk for AIDS: Haitians living in the United States, intravenous drug users, and people who required frequent blood transfusions. But no group was at greater risk than homosexual men. The first forty people diagnosed in the United States with AIDS were gay men living in California, Florida, Georgia, New Jersey, Pennsylvania, and Texas. To figure out how the AIDS virus—soon to be called human immunodeficiency virus (HIV)—spread, investigators constructed a diagram showing who had had sex with whom. In the center of the diagram was one man. All forty AIDS victims had had sex with this man or with someone who had had sex with him. They called him Patient Zero. His name was Gaetan Dugas.

Born and raised in Quebec, Dugas, a steward for Air Canada, traveled extensively throughout the United States, frequenting many gay bars and bathhouses. When he walked into bars, he would stand in the entrance, scan the room, look carefully at each patron, and declare, “I am the prettiest one.” And he was. Randy Shilts in
And the Band Played On
described Dugas as having “sandy hair that fell boyishly over his forehead, an inviting smile, and a laugh that could flood color into a room of black and white.” His sexual escapades were legendary. “In San Francisco,” wrote Shilts, “Gaetan returned from every stroll down Castro Street [the center of the gay community] with a pocketful of matchbook covers and napkins that were crowded with addresses and phone numbers. At times [he] would stare at his address book with genuine curiosity, trying to recall who this or that person was.”

Dugas was twenty-eight years old when a biopsy of an enlarging purple spot below his right ear revealed Kaposi's sarcoma—“gay cancer.” At the time, Dugas estimated that he had slept with two hundred and fifty men a year for ten years—twenty-five hundred sexual partners in all. Knowing that AIDS was contagious didn't stop Dugas from continuing to satisfy his sexual appetite. “Rumors began on Castro Street about a strange guy at the Eighth and Howard bathhouse, a blond with a French accent,” noted Shilts. “He would have sex with you, turn up the lights in the cubicle, and point out his Kaposi's sarcoma lesions. ‘I've got cancer,' he said. ‘I'm going to die. [And now] so are you.'”

 

A
FEW YEARS BEFORE
HIV
FIRST ENTERED THE
U
NITED
S
TATES
, M
AU
rice Hilleman began working on a new vaccine—not for HIV, which was still unknown, but for hepatitis. Because of the method he chose for making it, fear of AIDS would soon spread to fear of Hilleman's vaccine. For almost two hundred years, researchers had used cells from monkeys, chickens, mice, rabbits, and ducks to make their vaccines. Hilleman was about to break new ground. He would be the first (and last) to use human blood to make a vaccine. He didn't know until later that the blood was heavily contaminated with HIV.

Several viruses infect the liver. But by far the most common, the most severe, and the most feared is hepatitis B virus, which infects one third of the world's population, about two billion people. Most people infected with hepatitis B virus recover completely. But not everyone recovers. Some people die of an overwhelming infection in a matter of weeks. Others have a persistent infection: one million people in the United States and more than three hundred million people in the world are chronically infected with hepatitis B virus. And most of them don't know it. Victims of chronic hepatitis B are at high risk for two possible fates: dying of cirrhosis, a progressive destruction of the liver, or dying of liver cancer. Hepatitis B virus is the third most common known cause of cancer in the world. The sun, which causes skin cancer, is the first; cigarette smoking, which causes lung cancer, is the second.

 

B
EFORE
M
AURICE
H
ILLEMAN COULD MAKE HIS HEPATITIS
B
VACCINE,
he had to capture the virus. When Hilleman had wanted to make vaccines against measles, mumps, or rubella, he simply swabbed the throats of children with those diseases. Unfortunately, hepatitis B virus is barely detectable in saliva. Blood, on the other hand, contains extraordinarily large quantities of the virus—about five hundred million infectious particles per teaspoon. But blood from people infected with hepatitis B contains more than just virus particles. It contains something that will ultimately lead to the eradication of Every virus has a different strategy for survival. To avoid provoking an immune response that would destroy them, chickenpox and herpes simplex viruses live silently, latently, in the nerves. Many people initially recover from infection only to have these viruses reemerge decades later in the form of shingles or herpes blisters. Influenza virus outsmarts the immune system by constantly changing one of its surface proteins, the hemagglutinin. People make antibodies to the hemagglutinins of influenza viruses one year, only to find that these antibodies don't completely protect them the following year. So influenza virus continues to thrive. Rabies virus, which lives in saliva, evades the immune system entirely. After entering the body through the bite of an infected animal, it slowly, inexorably travels up the nerves of the arm or leg to the brain, moving from one nerve cell to the next, never entering the bloodstream. Many people infected with rabies virus make rabies antibodies. But by traveling from cell to cell, the virus effectively hides from antibodies in the blood. When rabies virus finally reaches the brain—a process that takes about two months but can take as long as six years—death is inevitable.

HIV is probably the most heinous because it infects one particular group of cells: T cells, which are important in directing the immune system. When T cells are destroyed, the immune system is disabled. Worse, HIV evolves rapidly during infection; people make antibodies to the virus only to find that different HIV viruses have taken the place of the old ones.

Hepatitis B virus has a strategy for survival that is different from that of any other known virus. In order for hepatitis B virus to infect the liver, it must first bind to liver cells via a protein that sits on the surface of the virus. People make antibodies against this viral surface protein to prevent the virus from attaching. If the virus can't bind to liver cells, it can't infect them. But hepatitis B virus fights back by making far more viral surface protein than it needs to make new virus particles, hoping that this excess surface protein will soak up antibodies from the blood and allow free virus to attach to liver cells. Hepatitis B virus is so committed to this method of survival that people infected with the virus have about five hundred quadrillion (500,000,000,000,000,000) particles of viral surface protein circulating in their bodies during infection. But hepatitis B virus's strategy of overproducing surface protein would eventually prove to be its Achilles' heel.

 

T
O MAKE HIS HEPATITIS
B
VACCINE,
H
ILLEMAN FOLLOWED A TRAIL
blazed by Baruch Blumberg, a researcher working at the Fox Chase Cancer Center in northwest Philadelphia. Blumberg wasn't a virologist, an immunologist, or an infectious disease specialist. He was a geneticist. For the longest time, while studying hepatitis B surface protein, he didn't have the faintest idea of what he was looking at.

A stocky, powerful, outgoing native of New York City, Baruch Blumberg got a degree in physics from Union College in Schenectady, New York, before attending the College of Physicians and Surgeons at Columbia University. The single event that changed his life occurred in the early 1950s between his third and fourth years of medical school. “Harold Brown, our professor of parasitology,” recalled Blumberg, “arranged for me to spend several months at Moengo, an isolated mining town accessible only by river, in the swamp and high bush country of northern Suriname [in South America].” Moengo was a melting pot inhabited by Javanese, Africans, and Chinese, as well as Hindus from India and Jews from Brazil. Blumberg found that people with different backgrounds had different susceptibilities to certain infections.

One infection common in Suriname was elephantiasis, caused by
Wuchereria bancrofti
, a tiny worm that blocks the flow of lymphatic fluid from the legs or genitals, causing massive, disfiguring swelling. Legs become coarse and thick, and scrotums become so swollen that victims have to carry them around in wheelbarrows.

Wuchereria bancrofti
causes severe elephantiasis in some people but mild or no disease in others. Blumberg found that susceptibility to diseases like elephantiasis could be directly linked to ancestry. He reasoned that people with different susceptibilities to a particular disease made proteins that served the same function—for example, to counteract the disease—but that these proteins were slightly different in their size or shape. They were thus known as
polymorphisms
, for “many forms.” Researchers had already found several protein polymorphisms. For example, they found that people have different proteins—A, B, and O—on the surface of their red blood cells. Blood group protein differences are important. If a person with type A blood receives type B blood, that person will make antibodies to the type B protein that destroy the transfused cells. The reaction can be massive and fatal. This is why doctors determine a patient's blood type before transfusion.

Blumberg's hypothesis that disease susceptibility is genetic is probably best shown by the origin and function of one specific type of hemoglobin, called hemoglobin S. Hemoglobin, a protein found inside red blood cells, also has several different forms. Fetuses and newborn babies have hemoglobin type F; most children and adults have hemoglobin type A; and some people, mostly of African descent, have hemoglobin type S. These three different hemoglobin proteins have the same function—to carry oxygen from the lungs to the rest of the body—but they are clearly different in size and shape. It isn't a coincidence that hemoglobin S is found mainly in people from Africa. People with hemoglobin S are better able to resist malaria—a parasite common in Africa—than are those with hemoglobin A. When the malaria parasites enter red blood cells, hemoglobin S eventually causes cells to change shape, making it more difficult for the parasites to survive. Unfortunately, some hemoglobin S–containing red blood cells, which look like tiny sickles, have difficulty passing through small blood vessels. The genetic adaptation to malaria infection is called sickle cell disease.

Looking for protein polymorphisms, Blumberg examined blood from people who had received at least twenty-five blood transfusions. He reasoned that people receiving many blood transfusions would be more likely to have antibodies to proteins different from their own. In 1963 Blumberg found that the blood from a man with hemophilia in New York City contained antibodies to a protein found in the blood from someone halfway across the world, an Australian Aborigine. He called the protein in the Aborigine's blood Australia antigen. (An antigen is a protein that evokes an immune response.) Blumberg found that Australia antigen was very rare in the United States—only one of every thousand people had it—but that it was quite common in tropical and Asian countries.

At this point, Blumberg didn't know what he had stumbled upon. Two years later, in 1965, Blumberg found to his surprise that Australia antigen was common in people with leukemia. He thought that the protein was either a marker for leukemia or part of a virus that caused leukemia. By 1967 he had found that Australia antigen, in addition to its presence in people with leukemia, was often present in the blood of Americans with Down syndrome. Again he thought that because children with Down syndrome were at higher risk for leukemia, Australia antigen was a marker for leukemia. But children with Down syndrome were more likely to have Australia antigen in their blood because they were more likely to have been infected with hepatitis B virus, the result of living in places like Willowbrook. Blumberg still hadn't realized that he had discovered a protein that was part of hepatitis B virus.

Eventually a virologist named Alfred Prince, working at a transfusion center in New York City, figured it out. In the early 1960s, Prince took blood from people before and after they received transfusions. In 1968, he found a patient who had hepatitis. Early samples of the patient's blood didn't contain Blumberg's Australia antigen, but later samples did. Prince concluded that “[Australia] antigen is located on a virus particle and the virus particle is etiologically related to some or all cases of serum hepatitis [soon to be called hepatitis B virus].” Prince was the first person to realize that Australia antigen was part of hepatitis B virus. Ten years later, in 1976, Baruch Blumberg won the Nobel Prize in medicine for discovering Australia antigen. His acceptance speech mentioned Alfred Prince briefly, parenthetically, and unfairly: “The Australia antigen association was also confirmed in 1968 by Dr. Alberto Vierucci, who had worked in our laboratory, and [that of] Dr. Alfred M. Prince.”