Origin of Deadlines of 1918 Flu Virus Is Found

Researchers at the University of Arizona say they may have discovered both the origin of the influenza pandemic of 1918 that left 50 million dead worldwide, as well as what may have made the virus especially deadly for 20- to 40-year-olds. The findings could be used to predict how vulnerable certain age groups are to future flu strains, offering potential insight into vaccination strategies and pandemic prevention.

Michael Worobey, a professor of ecology and evolutionary biology at the University of Arizona, and his team used a “molecular clock approach” to reconstruct the molecules that gave rise to the 1918 pandemic virus (known as H1N1 influenza A virus, or IAV), the classical H1N1 swine flu virus and the flu that circulated in the wake of the pandemic from 1918 to 1957. They found no evidence that IAV leapt directly from birds to humans, or that its emergence involved any sort of swap in genes between human and swine flu strains — two of the prevailing theories about the 1918 pandemic. Instead, they inferred that an H1 flu virus picked up genetic material from a bird flu strain. They believe, then, that the reason so many 20- to 40-year-olds were affected by the 1918 pandemic is because they had been exposed as children to another flu virus, H3N8, which circulated from 1880 to 1900. While their bodies developed an immunity to that earlier virus, H3N8 had a different antigenic protein than the 1918 H1N1 virus, which left that age group ill-equipped to fight off the new flu. Elderly people, by contrast, fared far better because they may have been exposed as children to an earlier H1N1-like virus, which means their immune systems would have been armed to repel the kind of virus that made up the 1918 flu.

“Imagine a soccer ball studded with lollipops,” Worobey explained. “The candy part of the lollipop is the globular part of the HA protein, and that is by far the most potent part of the flu virus against which our immune system can make antibodies. If antibodies cover all of the lollipop heads, the virus can’t even infect you.” Therefore, said Worobey, “a person with an antibody arsenal directed against the H3 protein would not have fared well when faced with the viruses studded with H1 protein. We believe this mismatch may have resulted in the heightened mortality in the age group that happened to be in their late 20s during the 1918 pandemic.”