Mounting efforts to make a vaccine to defend against a nasty, widespread bug likely just got tougher, with a Kiwi-led discovery challenging a long-held assumption about how our bodies try to fend off Strep A.
Mounting efforts to make a vaccine to defend against a nasty, widespread bug likely just got tougher, with a Kiwi-led discovery challenging a long-held assumption about how our bodies try to fend off Strep A.
Mounting efforts to make a vaccine to defend against a nasty, widespread bug likely just got tougher, with a Kiwi-led discovery challenging a long-held assumption about how our bodies try to fend off Strep A.
A common bacteria carried by many people, Strep A typically leads to mild throat andskin infections, but can also trigger potentially life-threatening diseases - especially when it turns into its invasive form.
It’s suspected to be involved in 500 such serious cases each year - including between 150 and 200 infections of the debilitating rheumatic fever – while annually costing the health system an estimated $59 million.
As scientists here and overseas push toward new vaccines for it, a University of Auckland-led study, just published in open-access scientific journal mSphere, has found a “one-size-fits-all” approach likely won’t work against it.
Study author and immunologist Associate Professor Nikki Moreland said her team had initially set out to understand how our immune systems try to combat infection.
“We looked at three major Strep A strain types and asked if the main protein, or antigen, on the outside of the bug that induces a protective immune response is the same, or different, for each strain,” she said.
“This is important to understand, as we need a clearer picture of how people develop immunity to the bug following infection to inform vaccine development.”
To answer that key question, the team tested the ability of antibodies from thousands of healthy adult donors to kill the different strains of Strep A in the lab.
University of Auckland immunologist Associate Professor Nikki Moreland.
“For many decades, it has been assumed that one protein on the Strep A bacteria, called the ‘M-protein’, is the main target of protective antibodies and immunity,” study author Dr Reuben McGregor said.
These protective antibodies were especially important, he explained, as they effectively “tagged” the bug for clearance by our immune system.
“We found striking differences in the role the M-protein had in the protective antibody response between strains,” he said.
“While the antibodies killed all the strains tested in the laboratory, we found that targeting the M-protein was key for killing some of the strains, but for others, it wasn’t involved at all.”
Those results came as a surprise, given it’d been assumed for decades that the M-protein was the main target for immunity for all Strep A strain types.
That the same team recently discovered New Zealand to be exposed to a “worldwide” population of the bacteria – known to contain more than 200 strains – made it all the more important to learn how our immunity varied with different forms of it.
“Our findings suggest that people develop immunity to Strep A by generating responses to different components of the bug depending on the strains they are infected with,” he said.
“For some strains, that will be the M-protein; for others, it will be another component of the bug entirely.
“It means a one-size-fits-all approach might not work for developing a vaccine against Strep A.
“It also opens the door to testing other components of the bacteria, beyond M-protein, that the immune system targets. There are vaccines in development directed to other parts of Strep A, and combining these components could lead to more effective vaccines in the future.”
Moreland said the team now planned to investigate more Strep A strains in depth.
“Mapping the different parts of the bug that are targeted by protective antibodies - and comparing these across the spectrum of Strep A currently circulating in New Zealand – will help in the design and selection of better vaccines.”
