Last Reviewed on May 13, 2020, by eNotes Editorial. Word Count: 1295
Chapter 3: From Sailors to Swine
In November 1918, Navy officials made sixty-two convicted Navy men an offer: if the convicts let doctors deliberately infect them with the flu, they would be pardoned for their crimes. Though such studies are illegal today, in 1918, “such ethical arguments were rarely considered.” The men accepted the offer, and doctors tried every way conceivable to infect them with the respiratory illness, including spraying their noses and throats with mucus collected from infected patients. Yet none of the volunteers contracted the flu, stumping doctors.
A vital clue about the 1918 strain came to light in 1928 through Dr. Richard E. Shope, a young scientist working on diseases in pigs with his mentor, Dr. Paul Lewis, at the Rockefeller Institute. While researching, Dr. Shope stumbled upon “the disease that was to become the consuming passion of his life: swine influenza.” Shope learned that at the start of the flu pandemic, millions of pigs in the American Midwest curiously died of an acute respiratory disease that resembled the human flu. Unable to accept this as a coincidence, J. S. Koen, a government official researching disease in pigs, declared in 1918 that swine and human influenza are “one and the same” and that pigs contracted the disease from humans. However, people were quick to dismiss Koen.
Dr. Shope, however, was intrigued by Koen’s findings. Investigating the flu in swine could, he thought, help unlock the mystery of the killer influenza. Dr. Shope and Dr. Lewis began to infect healthy pigs with microorganisms found only in flu-struck pigs. Dr. Shope’s results ultimately proved that the flu is spread by some unknown thing—apart from bacteria—in the secretions of sick pigs.
At the same time, in England, scientists Dr. Wilson Smith, Dr. Christopher H. Andrewes, and Sir P. P. Laidlaw were involved in a similar mission. After discovering that ferrets are susceptible to the human flu, they inoculated the animals with filtrate from human flu patients. Within days, the ferrets started showing symptoms of the flu. Further, the scientists showed that the disease can pass from sick to healthy ferrets and that ferrets can get influenza from both human and swine filtrate.
Continuing research from both groups of scientists found that animals inoculated with a human flu become immune to swine flu, and vice versa. Thus, antibodies from one strain of influenza may protect against another. But doctors still didn’t know which flu virus caused the 1918 pandemic. Dr. Shope and the British team decided to trace the virus through antibodies in the blood of survivors of the 1918 flu. Plasma from survivors was found to be full of antibodies that completely blocked the swine flu virus Dr. Shope had isolated. On the other hand, people born after 1918 did not have immunity to swine flu.
Dr. Shope believed that the two findings showed the footprints of the 1918 virus and its relation to swine flu. However, lingering questions about the flu could only be answered when scientists were able to obtain a sample of the actual 1918 flu virus.
Chapter 4: A Swedish Adventurer
The quest for that virus took a new direction in 1950 with a Swedish-born scientist named Dr. Johan V. Hultin, who worked at the University of Iowa. In the years since Dr. Shope’s research, pioneering work had been done on the influenza virus. Scientists found that the virus can grow inside chicken eggs, making it far easier to study. Scientists also learned that influenza has different strains, with the type A virus being the most common among humans. In 1941, it was discovered that flu viruses contain a protein called hemagglutinin, so named because it makes red blood cells clump together. In 1944, Americans became the first populace to be vaccinated against influenza, using viruses that had been grown in egg cells and then killed.
Even so, the actual 1918 virus had still not been found. Spurred by a senior scientist’s remark about the virus possibly being preserved in the lungs of a victim buried in the permafrost in North America’s northernmost reaches, Dr. Hultin decided to go to Alaska. His plan was to locate and dig up the bodies of flu victims, section their lungs, place the sections on dry ice, and bring them back to study. It was only in a cemetery in Brevig, the last site on his itinerary, that Hultin found some luck.
Digging into permafrost is physically arduous: the ground is hard and rubbery. Dr. Hultin improvised by keeping a constant fire at his digging site to soften the ground. Doing backbreaking work amidst smoke and melting ice, Dr. Hultin and his team finally excavated five bodies and cut them open, removing and freezing a “two-inch” cube of lung tissue from each.
However, back at the University of Iowa, the tissue samples failed to cause the growth of viruses in eggs. After struggling for months, Dr. Hultin turned to guinea pigs, then ferrets, applying “every trick of virology.” Not one animal was infected by the Alaskan samples. Because his study failed, Dr. Hultin never wrote up its results or authored a paper about it. He ended up practicing privately as a pathologist in San Francisco.
Meanwhile, other discoveries about the influenza virus continued. Scientists learned that the virus contains another protein, in addition to hemagglutinin: neuraminidase, which newly-made viruses use to burst out of a host cell in a spray so that they can affect nearby cells. Individual viral strains, such as H1N1, are ultimately named for these two proteins.
Dr. Hultin kept track of all these developments. Every time an outbreak occurred, he dreamed of returning to Alaska to restart his hunt for the virus—but he didn’t act on the impulse. Even so, he was sure that “sooner or later something would come up.”
Chapter 5: Swine Flu
Kolata explores a strange, unfortunate fallout of Dr. Shope’s research on swine flu. In February 1976, eighteen-year-old Private David Lewis died of a sudden illness at Fort Dix, New Jersey. His diagnosis—influenza with severe pneumonia—was concerning. The disease had been spreading at Fort Dix for a month already. Was Lewis’s death from what officials had presumed to be a regular cold actually a return of the dreaded 1918 influenza?
When seven samples from Fort Dix showed an unknown flu strain, Dr. Martin Goldfield sent them to the Centers for Disease Control and Prevention (CDC), where the strain was found to closely resemble Dr. Shope’s swine flu virus. With one of every four infected men at Fort Dix dying, the situation seemed “dangerously close” to the 1918 outbreak.
Federal health officials were in a bind. With a swine flu vaccine available, they wondered if they should inoculate the entire population of the US to prevent a repeat of 1918, but they also worried that the strain infecting Fort Dix was not swine flu. Virologists and physicians were asked to fly to Atlanta to discuss the dilemma at the CDC. Among the group were Dr. Edwin D. Kilbourne, the chairman of the microbiology department at Mount Sinai Hospital in New York; Dr. David Sencer, head of the CDC; Dr. John Seal of the National Institute of Allergies and Infectious Diseases (NIAID); and several top army colonels. Dr. Kilbourne pressed for a vaccination, since 1976 was expected to be a flu year, and work on the vaccine began.
Although doubts around the need for mass vaccination continued to be raised, especially with the strain not found in civilians near the area, Dr. Kilbourne worked hard to develop a fast-growing virus which could be used for a vaccine. Soon, the virus was sent to drug manufacturers around the United States. Despite the reservations of some prominent scientists, Dr. Sencer sent a memo up the federal chain of command that recommended the vaccine. President Gerald Ford approved the vaccination program.