In addition to the 84 flu-related pediatric deaths recorded so far, government data shows that nationwide influenza levels have reached what they were during the 2009 H1N1 pandemic.
To be sure, this doesn’t mean we’re in the midst of a pandemic. Rather, it means that levels of “influenza-like-illness,” measured by outpatient and emergency room visits, are as high as they were at the peak of the 2009 outbreak, Anne Schuchat, acting director of the U.S. Centers for Disease Control and Prevention, told reporters at a recent news conference.
But this raises the question: If we could beat deadly viruses like polio, smallpox and measles – why not the flu?
Coincidentally, this year also marks the hundredth anniversary of the “Spanish flu” pandemic, the 1918 global outbreak that killed an estimated 50 million people around the world. Public health has come a long way since then, so we’re not on track for anything even approaching that number this year.
But though scientists and the pharmaceutical industry are working hard to develop a “universal” flu vaccine that fights the virus’ constantly changing strains – with at least two potential candidates in early-stage trials in the U.S. and the U.K. – it may be years before they actually become an everyday reality.
Here, we try to explain why that is.
WHY IS THE FLU SO HARD TO BEAT?
This has to do both with the virus and its hosts – us.
If our immune system is a system of defense, then the thing between it and the flu might best be imagined as an epic war.
The flu’s end goal is literally to divide and conquer. Once it successfully enters our cells, it replicates and divides along with those cells, so it can spread through our bodies and claim victory.
But our bodies won’t go down without a fight, launched by the immune system.
This back and forth has led to an ongoing saga in which the flu keeps changing its outermost structure – in a process called antigenic drift – and different flu strains keep combining to form new strains – called antigenic shift – so that the virus essentially undermines and evades our immune system’s attacks.
According to Adrian McDermott, chief of the Vaccine Immunology Program at the National Institutes of Health, all of that shifting and drifting make complete eradication of the flu a massive challenge, at least until a universal vaccine is developed.
WHY ISN’T THE SEASONAL VACCINE 100 PERCENT EFFECTIVE?
It has to do with the flu’s inherent unpredictability. Going back to that war, the vaccine is sort of like a radio warning, alerting the immune system to the flu’s impending attack.
Scientists constantly monitor the flu’s movements around the world. They use that information to predict the predominant flu strains in the coming season, and formulate the seasonal vaccine based on that information. With the vaccine’s help, our immune system theoretically knows what to expect and has a chance to gear up its defenses.
The problem is, scientists have to decide what strains to use in the vaccine almost a year in advance, and the flu has many different strains. For example, this season’s predominant strain is a difficult-to-target H3N2 strain. Next season could be a different H3N2 strain. Or it could be an H1N1 strain. And the predominant strain could change from the time the vaccine is formulated to the time flu season rolls around, meaning our immune system might encounter a slightly different strain from the one it’s prepared for.
In other words, it’s sort of like the flu is fighting a 21st century war, but the vaccine is still delivering its message with last century’s technology.
Now scientists want to figure out how to make the vaccine more effective.
SO WILL THERE EVER BE A UNIVERSAL FLU VACCINE?
This depends on one’s definition of “universal.”
As McDermott notes, all those different strains mean a universal vaccine would have to cover a lot of ground by protecting against a broad range of flu strains.
And that’s just universal in one sense. There’s also “universal” in the sense that the vaccine protects us for more than one flu season. In a perfect world, that would be for life.
Perhaps it’s no surprise there are complications on that front, too. For example, the flu is so common that everyone is exposed to it at some point, either by infection or vaccination, says McDermott. But scientists strongly suspect that the earliest flu strains to which a person is exposed seem to affect their immune system’s flu response for the rest of their life.
An example of this is the 2009 pandemic. Public health experts initially expected older adults would be most affected by that pandemic, but it ended up being the other way around: CDC estimated that globally, about 80 percent of the deaths from that pandemic were in people younger than 65 years of age.
It seems likely that older adults had been exposed to some flu strain earlier in their lives that gave them some protection in 2009, McDermott says.
But as he notes, this is all new research. The precise ways in which early exposure affects future immune responses remain largely a mystery.
All this to say, a universal flu vaccine – however one envisions it – will be quite challenging to come by.
But though the challenges are many, scientists are using all of this new research – about the structure of the flu, the ways our immune system targets it and the ways our immune system remembers it – to try to achieve that all-encompassing vaccinal victory.