Our resident expert offers a primer on how the flu works, its wacky history, and why you—yes, you!—should absolutely get the flu shot every year.
It’s flu season. Half of your class is out sick. You approach the subway with trepidation (and lots of hand sanitizer) and glare at anyone who sneezes. The slightest hint of feeling “off”—a tickle in the throat, an unusually groggy morning—fills you with dread.
And all the chatter about flu—on the news, at the gym, overheard at work—doesn’t do much to make you feel in control. You might hear that this year’s flu is an especially bad one—or is it that it’s only bad for old people and babies? Someone says the flu shot “didn’t work” this year, so good luck not getting sick. Then there’s that one friend who claims that in his whole life, he never got the flu except for the year he got the shot. And the other who says she’s just the kind of person who gets it every year.
It can be awfully tough to sort out fact from rumor, so NYU Stories called an expert, Elodie Ghedin, of NYU’s Center for Genomics & Systems Biology and the College of Global Public Health, to help address our own questions and fears. Ghedin, a MacArthur Fellow, led a major NIH-funded project to map influenza genomes (sort of like the Human Genome Project, but for flu), and recently co-authored a paper in Nature Genetics about how minor flu strains—those not usually targeted by vaccines (more on that later!)—may play a bigger role in flu transmission than previously thought.
Below are some key points from her primer on how the flu works, its wacky history, and why you—yes, you!—should absolutely get the flu shot every year.
Think you have the flu? You probably don’t.
If there’s one thing that drives Ghedin nuts, it’s when people complain that they got the flu shot and then came down with the flu anyway. Most of the time, she says, this simply isn’t true: you might feel crummy, but that’s probably because you caught something else. Lots of viruses come with “flu-like” symptoms (aches, fever, runny nose, sneezing), but most people only get the flu—influenza—once or twice a decade.
Remember a time when you weren’t just sniffly and sore, but bedridden, “totally debilitated, and completely knocked out? That might have been the flu,” Ghedin says. “But in general, it’s not usually the flu that you have.”
And the only way to be 100% sure is to have a sample taken, usually from your nose, and sent to a lab for testing.
Still, there’s more than one flu to get.
It’s complicated. But here’s Ghedin’s “crash course in flu”: Influenza has two main types that infect humans: type A and type B. Type A is the tricky one, because it has lots of subtypes. Aquatic birds—“the reservoir for all the diversity” of flu, Ghedin says—carry about 130 combinations(!) of these, most of which (thankfully) haven’t made it to humans yet. But some have, and they’re doozies. H1N1, for example, is a subtype.
And within subtypes, there are strains. Once you’ve been exposed to a given flu subtype, your immune system develops antibodies against the virus so that you can control part of it, even when you’re encountering a new strain. That’s why, as with most cases of seasonal flu, “You still get sick, Ghedin explains, “but it doesn’t kill you.” But new subtypes entering the population are a big deal, because people’s immune systems don’t recognize them. That’s what happened in infamous Spanish influenza pandemic of 1918.
Ghedin’s recent paper took a look at a much more recent pandemic—from 2009 in Hong Kong. In the study, she and colleagues sequenced whole genomes from nasal swabs taken from confirmed 2009 Hong Kong H1N1 and H3N2 flu cases and their household contacts. They found that the sick people weren’t carrying just one strain of the viruses, but a mixture. And they found that this mixture—of both “major” and “minor” strains—was easily transmitted within households. This is significant because only the major strains—those found to be dominant all over the world in a given year—are put into the vaccine. The World Health Organization the Centers for Disease Control have “surveillance labs” where they sample for different strains of flu circulating in local populations. The catch? It takes about six months to make the vaccine, during which time the dominant strain can shift.
So it is possible that you could get the shot and still get the flu—just not as likely as the complainers make it sound. And the vaccine doesn’t make you sick.
That H1N1 you heard so much about in 2009? It was a descendant of the 1918 Spanish influenza that killed 50 million people.
Back when people were first infected with the H1N1 subtype of flu in 1918, Ghedin explains, they passed the disease on to pigs. As the decades passed, H1N1 evolved in humans, spawning different strains of seasonal flu to which anyone who’d been exposed to the 1918 version had partial immunity.
But it also evolved separately in pigs. “Then fast forward to 2009,” Ghedin explains, and “that H1N1 that had been in pigs, after going through all kinds of evolutionary processes, ended up being transmitted from a pig back into the human population.” And because the virus evolves more slowly in pigs than in humans (pigs don’t live as long as we do), it was much more similar to the 1918 flu than anything most of us alive today had been exposed to. That’s why the very elderly—those who’d been exposed to the 1918 flu or a close relative of it, back in the 1920s or 30s—didn’t get as sick as younger people did. They had more antibodies to protect themselves from it.
That’s actually the short version of an even longer story. The decades between 1918 and 2009 also brought a succession of new subtypes that created their own pandemics when they first appeared, with each one replacing its predecessor as seasonal flu. Then there was the rogue 1950s-era H1N1 strain that made a lot of young people sick when it re-entered circulation (after being accidentally released, one theory suggests, from a Russian or Chinese lab) in the 1970s. That H1N1 co-circulated with another subtype, H3N2, for a number of years—before finally being ousted by the new-old pandemic H1N1 (remember?) that effectively time traveled from 1918 to 2009 by way of pigs.
Got all that? “It’s a very strange history,” Ghedin admits. And it makes designing a flu vaccine each year seriously tricky business: Scientists must decide which strains of each subtype to put in the vaccine (which can hold just three or four strains).
There’s a lot yet to learn about the role the different strains play in flu transmission (and in making you feel terrible)—hence the need for more studies like Ghedin’s.
In the ongoing worldwide war on flu, one longed-for weapon, Ghedin says, would be a sort of “universal” vaccine that could teach your “immune system to recognize a region of a virus protein that doesn’t mutate”—meaning it’s identical across all different strains. But scientists haven’t had much luck with that yet.
In the meantime, it’s important to get the regular flu shot every year. It’s the best defense we have now—and getting it can prevent you from passing the flu on to someone more vulnerable.
What about antiviral drugs?
Ghedin says that by the time you’re sick, antivirals probably won’t do you much good.
The only antiviral drugs that work at all these days, she explains, are called neuraminidase inhibitors, and they can’t do much once you’re already showing symptoms. To understand why, you have to know a bit about how the flu works.
The surface of the virus, Ghedin explains, has two proteins: hemagglutinin and neuraminidase (the “H” and “N” in H1N1). Hemagglutinin helps the virus get into a cell. “But once the virus has gone into the cell and hijacked the cell to make copies of itself,” Ghedin says, “there are new little viral particles that start budding off the surface of the cell like little oil drops.” Neuraminidase acts like a scissor that cuts those new viral particles loose so that they can go on to infect other cells. A neuraminidase inhibitor prevents that process—the viral particles bind to the already-infected cell and die there before they can move on and multiply.
“You want that inhibitor to be applied early on, when you just have a few cells that are infected,” Ghedin says, because the virus multiplies quickly, causing inflammation and the immune response that makes you feel miserable. “Your symptoms usually start two days after you’ve been infected, when you have the highest number of viruses in your body. So it's practically too late at that point.”
Ideally, to keep from feeling sick, you’d need to take the neuraminidase inhibitor after being exposed to someone who has the flu (say, when your spouse comes home from work sick), but well before you started feeling symptoms yourself—a pretty narrow window. Plus, Ghedin cautions, it’s important to limit the prescription of antivirals to those who could die from the flu, because drug resistance develops quickly in flu viruses.
And if you get sick, please, please stay home.
As anyone who’s ever silently cursed a coughing coworker may have suspected, respiratory viruses can be very contagious, and flu is no exception. “When you sneeze,” Ghedin explains, you project fine particles of a few different sizes. The biggest ones, like water molecules, fall to the ground right in front of you, while medium-sized particles travel about three feet. “But then there’s a fine mist that can go 20, 30, 40 feet or more,” Ghedin says, “meaning that you can easily contaminate a whole room when you sneeze.”
That’s seriously bad news for your colleagues, friends, and fellow commuters on a crowded subway car—especially infants, pregnant women, the elderly, and others (such as people with asthma) at risk of developing life-threatening complications with flu.
Oh, and those masks people wear to prevent infecting others? They’re good at stopping bigger droplets, but unless they’re worn very tightly around the nose and mouth, Ghedin says, the smallest particles can actually squeeze past the mask and onto the side of the face...and then out into the world. Yuck.