The just-ended 2018-2019 flu season was relatively mild compared to the last season, during which nearly 80,000 people in the U.S. died of flu-related illness, according to estimates by the U.S. Centers for Disease Control and Prevention.
This year’s death toll is predicted to be about half, or, in the worst case, three-quarters of that number.
The 2018-2019 season has been unusual, though, because the flu came in two waves: one that peaked at the end of December, and a second that peaked in early March. The two peaks were caused by two different strains of the flu virus, and the protection given by vaccination early in the season may have waned by the time the second strain appeared.
Flu epidemics reoccur every year because of the the way the virus is built and how it interacts with the human immune system. The viruses are highly changeable, acquiring genetic variations, called mutations, even within a single season. The new properties conferred by these mutations can allow the virus to evade the immune response elicited by the flu vaccine.
In addition, the immunity conveyed by a flu shot does not last from year to year. In fact, depending on the flu strain that is circulating, immunity may not even last through one flu season.
Here’s how it all added up over the flu season that has just drawn to a close.
When you’re first exposed to the live flu virus, your immune system shifts into gear to try to fend off the invader. Specialized white blood cells, called B-cells, make antibodies that attack two proteins that poke off the surface of the virus, preventing them from doing their jobs. These viral surface proteins, called haemagglutinin (HA) and neuraminidase (NA), are necessary for the virus to survive.
Your immune response may not be fast enough to stop the virus from successfully invading your respiratory tract cells and causing flu symptoms. However, over the course of the infection different parts of the virus evoke an immune response that is more extensive and longer lasting.
Once the infection is over, special cells, called memory B-cells, lie dormant, waiting for a second invasion of the same virus. If they recognize the previously fought flu virus, they launch a rapid immune response.
Vaccines are designed to get your immune system ready to confront a virus without having to first be infected to learn about it. Every year, the World Health Organization predicts which flu strains will circulate and vaccines are formulated with the anticipated strains.
Almost all current flu vaccines are made with killed virus. After injection, most of the antibodies made by the immune system’s B-cells are directed toward the “head” region of HA, the part that’s sticking furthest off the protein stalk from the surface of the virus. These antibodies prevent subsequent infection because the HA head is what makes first contact with the cells of the respiratory tract.
Because the dead viruses in the vaccine do not infect and grow, the wave of antibodies they induce is fairly short-lived and the vaccine is not great at creating memory cells. The challenge to your immune system from the vaccine is much more limited than if it were facing a full-on onslaught of live viruses.
That short memory is one reason why you need to be vaccinated every season – even if the same virus is circulating, your immunity to it may be gone by the next year.