Over two decades of research led by the University of Tampere in Finland has already provided solid evidence linking a type of virus called coxsackievirus B1 with an autoimmune reaction that causes the body to destroy cells in its own pancreas.
The type 1 form of diabetes – not to be confused with the more prevalent type 2 variety that tends to affect individuals later in life – is a decreased ability to produce the insulin used by the body's cells to absorb glucose out of the blood.
This loss of insulin is the result of pancreatic tissue called beta cells being destroyed by the body's own immune system, often within the first few years of life.
It's something of a mystery as to why the body identifies beta cells as foreign, though there could be a genetic link producing variations of human leukocyte markers, which act as the cell's 'ID tags'.
No doubt it's complex, and there are numerous ways this process can be triggered. One example established by virologist Heikki Hyöty from the University of Tampere is an infection by a type of enterovirus.
Enteroviruses are nasty pieces of work; you might be most familiar with polio, but they can also cause hand, foot and mouth disease, meningitis and myocarditis. There has been suspicion of a link between this group of pathogens and diabetes for a number of years, but it took time to nail down the prime suspects.
In 2014, Hyöty and his team used a pair of studies on Finnish children with type 1 diabetes to show that at least one of the six viruses in the B group of coxsackieviruses was associated with the condition.
Enteroviruses are surprisingly common in newborns, with the Centres for Disease Control and Prevention (CDC) finding that around a quarter of the 444 known enterovirus infections in the US in 2007 were caused by coxsackievirus B1 (CVB1).
And for some of those children, it could have been the start of a life-long, incurable condition.
"One can estimate from the generated data that less than 5 percent of CVB1-infected children go on to develop type 1 diabetes," the researchers wrote in their 2014 study.
That might not seem like a lot, but it does suggest each year hundreds of infants around the globe develop type 1 diabetes. If the other members of the CVB group also contribute to beta cell autoimmunity – which they might – the numbers could be higher.
If all goes well, this newly developed vaccine could put a stop to that.
"Already now it is known that the vaccine is effective and safe on mice," says Hyöty.
"The developing process has now taken a significant leap forward as the next phase is to study the vaccine in humans."
Pre-clinical trials are of course just the first step. The next phase will involve testing on healthy adult humans, just to map out any complications.
As a bonus, the vaccine could help reduce other enterovirus infections.
"Additionally, the vaccine would protect from infections caused by enteroviruses such as the common cold, myocarditis, meningitis and ear infections," says Hyöty.
It could be another eight years before we see whether the vaccine does what it's supposed to do, so we shouldn't be expecting anything revolutionary too soon.
Meanwhile, groups like the Juvenile Diabetes Research Foundation (JDRF) are continuing to fund research into finding better ways to prevent and treat type 1 diabetes by improving technology that mimics the function of the pancreas or by identifying ways to regenerate insulin-producing cells.
Earlier this year, researchers identified an immature cell in the pancreas which can potentially be encouraged to take up the job of lost mature beta cells.
There will be no single cure, treatment, or prevention which will gives us a diabetes-free world.
Between 20 and 40 million people worldwide live with type 1 diabetes. A vaccine like this might not end the disease, but if it works it's certainly going to be a big step forward.
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