Contagion was high on the box office list again last weekend, proof that millions of Americans are entertained by scenes of infection, suffering, sniffles and autopsies of Gwyneth Paltrow’s brain. The movie can sometimes veer a little over the top — in it, global society essentially melts down — but the risk of a dangerous new disease is no fiction. In fact, we’ve already experienced it.
The 1918-19 influenza pandemic, otherwise known as the Spanish flu, killed at least 50 million people worldwide, and potentially far more. During the worst months of the pandemic, cities shut down while accumulating bodies were buried in mass graves. The infection disproportionately carried off the young and the healthy, and death sometimes came in a matter of hours, as this 2007 story from Popular Mechanics described:
Deep brown spots would appear on a victim’s cheeks and a thick, bloody fluid would begin to overwhelm his lungs. Starting at the ears, their faces would gradually turn blue as circulating blood could not get oxygenated. Soon, victims would start to drown in their own fluid — often coughing up a pinkish froth as they fought to inhale. “It is only a matter of a few hours then until death comes, and it is simply a struggle for air until they suffocate,” an army doctor, based outside of Boston at Camp Devens, wrote to a colleague in 1918. “It is horrible.”
The Spanish flu pandemic was an outlier; influenza, as we saw with the relatively mild pandemic in 2009, is rarely a mass killer. So what made the 1918 virus so deadly? That’s a question the virologist Jeffrey Taubenberger has devoted much of his career to answer. Taubenberger led the team that was able to isolate and sequence the 1918 virus, taking tissue samples from the corpse of an Inuit woman whose body had been preserved beneath the permafrost in Alaska. That work would prove incredibly valuable (researchers were able to use it to trace how the virus changed as it jumped from birds to humans), but it couldn’t pinpoint exactly what made the 1918 virus so deadly.
Now Taubenberger is back with another flu study. Historians know that although flu cases first began to pop up in the spring of 1918, the real killer wave of the pandemic didn’t begin until the fall of that year. So scientists have wondered whether the virus might have undergone some important changes between the spring and the fall that made it deadlier and more transmissible, or even whether the first round of cases might have been caused by another virus altogether.
In a study published in the Sept. 19 Proceedings of the National Academy of Sciences, Taubenberger and his colleagues at the National Institute of Allergy and Infectious Diseases (NIAID) examined lung tissue from 68 American soldiers who had died of respiratory infections in 1918. They found proteins and other genetic signs of the Spanish flu virus in 37 soldiers, including four soldiers who had died between May and August 1918, well before the pandemic took off. Those four cases are the earliest known 1918 flu cases ever to be documented, which gave Taubenberger a chance to see how much the virus had changed over the summer.
Not much, as it turns out. The clinical disease and tissue damage seen in the pre-pandemic cases were virtually identical to that seen in the cases that occurred during the worst months of the pandemic. While it’s possible that the virus might have still been mutating in the spring of 1918 — strains from some of the early cases still show genetic receptors that bind to bird cells, while later strains are primed for human cells — there’s little evidence that the virus became more virulent over those months.
Taubenberger told Helen Branswell of the Canadian Press that the mystery of the 1918 flu virus’s lethality is still unsolved:
The answer to the mystery of why the 1918 virus killed tens of millions of people, especially young healthy adults, does not apparently live in the tissues that we look at under the microscope.
Because it happened once and we would certainly not want to see something like this happen again. So everything we can do to understand the past will help us prepare for the future.
Perhaps that’s what makes emerging infectious diseases so scary. Despite all of our scientific knowledge and experience, we still can’t fully understand a microscopic pack of eight genes, can’t figure out why one microbe is benign and another is murderous. And we know there are more out there waiting to be discovered — or to discover us.
It’s almost the stuff of a good horror movie.