Flu vaccine for the year 2014-2015 wasn’t as effective as its predecessors and researchers have finally revealed the reason behind that. According to a study published in Cell Reports just a single mutation in the flu virus helped it gain an upper hand over the vaccine.
According to the Centers for Disease Control and Prevention, last season’s flu vaccine was less than 20% effective at preventing medical visits associated with seasonal influenza illness, compared with up to 60% effectiveness of other seasonal flu vaccines during the past 10 years.
Although previous studies revealed a mismatch between the H3N2 vaccine strain and most H3N2 strains circulating in the Northern Hemisphere during the 2014-2015 season, until now, it was not clear exactly which viral mutations were responsible for this mismatch.
To answer this question, Scott Hensley of the Wistar Institute and his team applied a reverse-engineering approach to convert the 2014-2015 H3N2 vaccine strain into a panel of H3N2 strains with hemagglutinin mutations that are present in currently circulating H3N2 strains. They then examined whether these viruses would be recognized by antibodies present in blood samples taken from ferrets and sheep that had been exposed to the H3N2 vaccine strain. They found that a single mutation in the F159S amino acid residue of hemagglutinin decreased antibody recognition by as much as 75% compared with antibody recognition of the unaltered H3N2 vaccine strain.
The researchers then performed tests with blood samples taken from humans before and after immunization with the 2014-2015 vaccine. They found that vaccination was significantly less effective at increasing antibody recognition of the F159S-mutant strain compared with the unaltered vaccine strain. Taken together, the findings show that a single viral mutation could largely explain the ability of flu strains to get past the 2014-2015 flu vaccine.
“We find that some human immune responses are heavily focused on single regions of the flu virus and that single viral mutations can evade these immune responses,” Hensley says. “Influenza viruses might have evolved in a way that promotes the generation of narrow immune responses that are easy to circumvent via single viral mutations.”
Hensley and his team are now examining whether the new 2015-2016 H3N2 vaccine strain elicits robust immune responses to the different types of H3N2 strains that are currently circulating. To guide the design of subsequent vaccines, they are also attempting to predict how flu viruses might mutate in the future.
In the meantime, Hensley urges the public to continue to get annual flu vaccines. “Most years, vaccine strains are well matched to most circulating strains, and seasonal flu vaccines are usually more effective,” he says. “The best way to prevent flu infection is by getting a flu vaccine.”
