We have learned a lot from the 2009 H1N1 swine flu pandemic.
We have learned, for example, that one basic assumption about pandemics was wrong: You don’t need a radical mutation in a flu virus to produce a pandemic. All you need is enough change within a surface protein for a new strain to blow past acquired immunity and blaze around the world, as this one did.
And we’ve seen that not every pandemic strain is especially lethal. The Centers for Disease Control and Prevention in Atlanta estimated that 11,690 Americans had died of swine flu by mid-January. In a “normal” flu season, the CDC estimates that 36,000 Americans die.
As Peter Palese, an eminent flu virologist from Mount Sinai Hospital in New York, put it, “We were lucky -- this was a mellow virus.” It lacks the virulence factors that make highly pathogenic bird flu, or the 1918 pandemic flu virus, so deadly.
In the beginning, the pandemic seemed to have an ominous affinity for the young. But this turned out to be mostly a matter of resistance. Many people born before 1957 have some cross-immunity to the virus because of their exposure to a previous H1 outbreak. So older people -- the usual victims of seasonal flu -- caught the new virus at much lower rates. And even among young people, though the attack rate was ferocious and many millions were infected, only a tiny percentage of those who got the flu died.
Another thing we’ve learned is that a safe, effective new flu vaccine can be produced fairly rapidly. In 1976, when 40 million people were quickly immunized against a pandemic that never came, several hundred of those receiving inoculations fell ill with Guillain-Barre paralysis, leaving Americans skeptical about fast-turnaround vaccines. This year was different.
“We’ve had intensive safety monitoring because of the experience with 1976,” said Anne Schuchat, director of the CDC’s National Center for Immunization and Respiratory Diseases, adding that “the safety record looks fantastic.”
On the other hand, we have learned more about the virulence of the anti-vaccine lobby, which persuaded far too many people not to get vaccinations or -- even worse -- not to vaccinate their children. Dr. Paul Offit, chief of infectious disease at Children’s Hospital of Philadelphia, worries that the anti-vaccine fringe has gained the upper hand and is calling the shots on some important matters of public policy.
For example, he notes, no one in America dared put adjuvants -- immune-stimulating chemicals -- into the vaccine, a move that would have stretched the limited supply. Both Canada and Europe used the chemicals with no ill effects. In Europe, vaccine makers use the adjuvant squalene, which means that children need only one shot instead of the two required here. But say the word “squalene” and multitudes of Americans shudder: Squalene in anthrax shots has been fingered by some anti-vaccine activists as the cause of Gulf War Syndrome. That squalene is a chemical precursor to cholesterol and produced in the body every day -- and that you can even find it in Girl Scout cookies -- means nothing to them.
Though H1N1 transmission appears to be dying down, we surely haven’t seen the last of this virus. Some experts, including flu virologist Michael Shaw of the CDC, fear that the virus could evolve around existing immunity, leaving the elderly vulnerable.
Perhaps the most important lesson we can still learn from this pandemic is where it came from and how we can prevent another one. Columbia University virologist Raul Rabadan, who has studied rates of mutational change in swine, bird and human flu, says that the current pandemic virus most likely emerged from a pig herd. Circumstantial evidence points to a giant, high-density pig farm in the small (3,000 people) town of La Gloria, in Veracruz, Mexico, where, according to an Associated Press report, about 450 people were diagnosed in late March with acute respiratory infections. There too the pandemic’s “index case” -- Edgar Hernandez, a 5-year-old who first tested positive for H1N1 -- was identified.
Gregory Gray, a University of Florida influenza researcher, has shown in several studies that 12% to 21% of Iowa pig farmers have antibodies to H1 pig influenza viruses. His team’s studies suggest that workers may pass these infections on to their families. But generally the pig viruses stop there.
This one didn’t. Edgar had no contact with pigs, nor had his family. No one knows what gave this pig strain wings. Still, there must have been some point after H1N1 had jumped into people at which transmission was still sluggish, when the virus had not yet adapted to spread efficiently from person to person, when the pandemic could have been aborted. But no one was looking.
If we have any hope of stopping another pandemic, it lies in monitoring the animal-human nexus, particularly on large farms, which can function -- as 12 years of experience with highly pathogenic bird flu in Southeast Asia has shown us -- as factories for lethal disease. Packing animals together allows the evolution of virulent pathogens, as deadly germs can easily spread from one animal to its neighbor. The H5N1 bird flu never evolved the ability to transmit effectively from person to person.
But swine flus seem to adapt more quickly to human beings, perhaps because pigs and people share similar flu receptors.
We need to closely watch high-density pig farms and monitor their workers for signs of illness before another pig virus -- perhaps one less mellow -- bursts out and sweeps across the Earth again.
Wendy Orent is the author of “Plague: The Mysterious Past and Terrifying Future of the World’s Most Dangerous Disease.”