This is the second article in a four-part series on fading immunity to Covid-19 and the flu—the science behind it, and the implications it has for vaccine development and the pandemic at large.
One of the reasons we get flu shots annually is because new strains of influenza emerge and circulate year in and year out. But another reason, a new study shows, is that vaccine-induced antibodies against influenza tend to fade relatively quickly, most within a year or less.
For many of us, this likely comes as a surprise. If we’re vaccinated against a particular strain of influenza, we’d expect any protective immunity we gain to at least ward off the same strain the following year. Evidently, this isn’t the case—a discovery that gains all the more significance now that fast-fading immunity appears to be a defining, though still perplexing, feature of Covid-19.
The study in question, published in Science magazine earlier this month, examined the activity of bone marrow plasma cells which play a critical role in sustaining the body’s long-term antibody response, in 53 volunteers who were vaccinated between the years 2009 and 2018. While the number of bone marrow plasma cells produced in patients as part of their natural immune response remained fairly consistent over time, those induced by vaccines declined to baseline levels after one year.
Perhaps the most immediate implication of these findings, at least in the realm of influenza research and clinical practice, is that the optimal time for vaccinating against the flu might be later than previously thought. A 2018 study reached a similar conclusion, but by alternate means, focusing specifically on vaccine efficacy within the span of a single flu season. People vaccinated later in the season were less likely on average to eventually test positive for the flu—a correlation that runs contrary to the general assumption that when it comes to getting your flu shot, the earlier, the better.
The broader implications extend to the current pandemic and the ongoing race to develop Covid-19 vaccines. While SARS-CoV-2, the virus that causes Covid-19, doesn’t mutate nearly as much as influenza viruses, recent research shows that the antibodies we produce to fight it can dwindle to undetectable levels in mere months. The challenge faced by any vaccine candidate, then, is to outperform the immune system in this regard. Yet even with flu vaccines, the Science study tells us, this has yet to be accomplished.
Several of the Covid-19 vaccines either undergoing large-scale clinical trials around the world or being administered in China and Russia are manufactured using adenovirus vectors, a technology designed to trick the body into activating its defenses by slipping a sliver of genetic material from SARS-CoV-2 into a run-of-the-mill cold-causing virus. Until now, no such vaccine has been brought to market that prevents disease in humans. Even if one of these candidates becomes the first, it won’t have a particularly long shelf life; once the body begins making antibodies to the adenovirus vector itself, it can not be used as a booster the following year.
Try as we might, we cannot continue to create goals and timelines for Covid-19 vaccine development—much less vaccine distribution—that gloss over the immunological complexities that make this virus, and our attempts to protect ourselves from it, so problematic. Thanks to scientific and medical progress we’ve made since SARS, the first coronavirus pandemic, we already know an impressive amount about SARS-CoV-2. Yet a sizable gulf remains between what we know and what we’re doing in response. In the next part of this series, I will discuss another phenomenon that will affect our ability to develop and deploy vaccines against Covid-19—autoantibodies.