Everyone has their own unique response to the flu – vaccinated or not – researchers found as they worked to uncover the flaws in the shot.
This season’s flu vaccine was only about 36 percent effective overall and only 25 percent effective against the predominant and deadly H3N2 strain.
As was the case during the 2012-2013 flu season, many experts have raised concerns that the strain used to make the preventative medicine had mutated during its production in eggs, rendering it ineffective.
However, new research from the University of Chicago and Harvard University has shown that flu vaccine’s effectiveness may depend more on what flu strains you’ve been exposed to over your whole life than on what is in the shot.
The vaccine’s effectiveness is likely more dependent on a person’s personal immune history than on mutations that occur during the shot’s mutations during production, research reveals
But researchers from the University of Chicago and Harvard University found that every person had their own unique response to the flu – vaccinated or not.
The flu has killed at least 84 children this season, and 20 percent of them were vaccinated, according to the Centers for Disease Control and Prevention (CDC).
Statistics like these leave parents and the public at large frustrated, feeling helpless against an epidemic that returns each year, without fail.
Health officials called the shot’s ineffectiveness early on: initial estimates said it would be about 40 percent effective, then as low as 30 percent. Last week’s figures showed it to be 36 percent effective for adults overall, but only 25 percent effective against H3N2.
The CDC found that children fared better – the shot was 59 percent effective against H3N2 for them – but kids are also more susceptible to infection in the first place.
Many have decried the vaccine’s production method, as they did the vaccine for in the 2012-2013 flu season that killed 170 children and was only estimated to be 39 percent effective.
Each year, a number of candidate vaccine viruses are selected and injected into eggs where they are incubated and replicate, or multiply, for several weeks.
During this period, like any living thing, the virus cells are liable to mutate before the antigens – the part of a virus that provokes an immune response – are extracted.
These antigens put the immune system on high alert for that particular strain of a virus, so that the body is primed to attack it over any other pathogen.
If the antigens come from a mutated virus, they may not provide the correct preventative immune response.
Many experts concluded that this was why the 2012-2013 season vaccine did not work very well and suspect the same was true of this year’s relatively inadequate shot.
This theory was supported when researchers gave ferrets that had never previously had the flu both the vaccine and the illness in 2013.
Their naïve immune systems were able to detect the differences between the two, the vaccine was ineffective and the eggs got all the blame for creating a mismatched virus.
But the findings of the new study suggest that the eggs may not be at fault at all.
Instead, the vaccine may falter over a phenomenon called the ‘original antigenic sin.’
According to this theory, your immune system will tend to respond to anything that resembles the first exposure the same way.
The study authors Dr Sarah Cobey of the University of Chicago and Dr Yonatan Grad the TH Chan School of Public Health at Harvard exposed blood samples from people who had and had not been vaccinated for the 2012-2013 season to the H3N2 virus.
Essentially, the vaccine itself made little difference.
‘We see that both vaccinated and unvaccinated people were infected with similar flu viruses and that the vaccine didn’t elicit a strong immune response from most people in our study,’ said Dr Grad, an assistant professor of immunology and infectious diseases at the Harvard TH Chan School of Public Health.
Instead, the human immune system seems to pick up on the presence of a flu strain – from either the vaccine or the flu itself – and respond as if it were whatever the first strain it encountered had been.
‘Imagine influenza viruses are like different makes and models of cars,’ said Dr Grad. ‘The ferrets, which hadn’t seen influenza before learned to tell the difference between closely related strains – like telling the difference between a Honda Civic and a Toyota Camry.
‘But people didn’t distinguish between them and just saw cars.’
Missing the Camrys for the cars elicited a weak immune response, but ‘the mechanisms underlying [that] are unclear but incredibly interesting and important,’ Dr Grad told Daily Mail Online.
So the vaccine’s egg mutations and viral mismatching may matter, but ‘sometimes they matter and sometimes they don’t, but what seems to make the most difference is immune history,’ says Dr Cobey.