Learn how immunizing a critical portion of a community protects most members of the community.
Ena Grant was only 9 months old when she started to walk. Two months later and feverishly sick with the flu, she constantly screamed when she tried to walk and found she could no longer take any steps. It would not be until well after her first birthday when little Ena would walk again.
It was November 1918 when one of the worst influenza pandemics in U.S. history struck Atlantic Mine, MI, where Ena's family lived. Although she became infected, she survived; two of her sisters were not so fortunate. Bertha, who was 3, died from influenza on a Friday. The next day, 9-year-old Alexi passed away. When the sisters were buried on Sunday, a third grave was dug for Ena after the family physician told her parents that he was convinced that the baby would also not survive.
Now 88 years old and living in Birch Bay, WA, Ena Grant remembers nothing of her firsthand experience with the deadly 1918 flu, only what little her parents told her.
“With a large family to care for and no newspaper or television, I don’t know if they were really aware of what was going on, or aware that it [the flu] was sweeping the country,” she says. She only recently began thinking of her brush with the deadly flu after seeing news reports of the H5N1 avian flu virus sweeping through Southeast Asia.
Interestingly, neither of her parents nor her 5-year old sister Gertrude became sick with the 1918 flu. Ena credits her own survival to the fact that she was still nursing when she became ill with the flu and, therefore, she must have acquired some of her mother’s protective immunity to the virus.
Dina Friedman, Ena Grant’s next door neighbor and friend, also has a family history with the 1918 flu: her grandfather and an aunt on her father’s side succumbed to the virus. At the time, her father, Arthur W. Peterson, and her uncle, 24-year-old Al Peterson, were in the Navy. They were stationed on the East Coast when they learned that their father had died from the flu. When they returned to Spokane, Washington, to attend to their father’s affairs, they discovered that their 22-year-old sister Sigrid, who had traveled from California to care for their father, also had died, according to Dina Friedman.
Friends had already buried their sister. However, to locate their father’s body, the two grief-stricken brothers had to sift through dozens of bodies of flu victims that had been spread out in a large local gymnasium.
Aside from the enormous horror and sadness of that situation, what is amazing to Dina Friedman is that her father and uncle never got sick with the 1918 flu. “They lived in a heavily populated area and were surrounded by Navy men who were constantly coming and going. They had hundreds of contacts and, therefore, should have been exposed to the flu many times over. But they didn’t get it,” she says.
What makes someone immune to such a deadly virus while so many others, particularly younger people, died in massive numbers? And can 1918 flu survivors, such as Ena Grant, offer some clue to protecting against another deadly flu pandemic?
Those are the questions Christopher F. Basler, Ph.D., assistant professor of microbiology at the Mt. Sinai School of Medicine in New York City, is trying to answer. By collecting and examining blood samples from 1918 flu survivors, Dr. Basler is trying to understand what made the 1918 influenza virus so deadly and how vulnerable today’s population would be to a similar virus.
Through the blood samples, Dr. Basler and his research team are hoping to recover B cells, the cells responsible for helping produce a human immune response. In this case, they are specifically looking for “memory” B cells, those cells exposed to the 1918 flu virus and, therefore, likely capable of producing antibodies if exposed to a similarly constructed virus.
Using a technique developed in 2004 to identify antibodies capable of destroying the SARS virus, Dr. Basler and his research team plan to take B cells recovered from 1918 flu survivors and attempt to identify those that make antibodies specifically targeting the 1918 flu virus and examine the antibodies the cells produce. In this way, they hope to identify those antibodies capable of neutralizing the 1918 flu virus.
“Finding antibodies against the 1918 virus should be easy. It’s isolating those memory B cells specific to the 1918 flu virus that will be the hard part,” Dr. Basler says. “They’re not likely to be circulating very heavily in the blood, and trying to identify them and culture them is like finding a needle in a haystack.”
The project, which is being funded by the National Institute of Allergy and Infectious Diseases, also involves an investigation into the virulence of the 1918 flu virus’ surface proteins: hemagglutinin, which allows the virus to stick to a cell and cause infection; and neuraminidase, which enables newly formed viruses to escape the host cell. Because the influenza A virus strain that caused the 1918 pandemic is now extinct in nature, Dr. Basler and colleagues have reconstructed the individual genes of the virus using sequenced 1918 gene data and reverse genetics techniques with the intention of studying the function of the genes within recombinant flu viruses. The hope is that these studies will not only illuminate the workings of the 1918 influenza virus but also provide insight into all human flu viruses.
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Last Updated July 08, 2009