Are viruses using a sneaky disguise to enter beta cells?
Posted on 10 August 2018
Viruses may be using empty insulin sacs as a disguise to sneak into beta cells and infect them new research suggests.
Beta cells release insulin in sacs. Once emptied, the sacs are then recycled back into the cell.
This research suggests that certain viruses could be using the empty sacs to stow away into the beta cell.
The work was partly funded by JDRF.
Why did they do this work?
Researchers suspect that certain viruses called enteroviruses may play a role in the development of type 1 diabetes. Enteroviruses normally only result in cold-like symptoms, but they have also been found in beta cells of people with type 1 diabetes.
Viruses need to enter cells in order to make more copies of themselves. They usually enter cells by exploiting existing cell machinery, for example by binding with certain receptor proteins that carry out other essential functions for the cell.
If we can understand how enteroviruses enter and remain in the beta cells, it could help us to develop treatments to combat enterovirus infections. This could in turn potentially protect people from developing type 1 diabetes.
The team of researchers, led by Dr Sarah Richardson at the University of Exeter, therefore investigated where exactly the receptor proteins for enteroviruses are in beta cells.
What did they find?
The researchers studied various pancreatic samples from people with type 1 diabetes as well as from those without.
They found that the receptor protein that enteroviruses like to bind to is found inside the cell, rather than on the surface as previously assumed. In addition, their data suggests that the receptor protein is found inside sacs of insulin.
What does this mean for type 1?
The researchers propose that viruses make use of the insulin sacs to enter beta cells in disguise.
When the sacs of insulin are released from a beta cell, the viruses recognise the receptor proteins inside and use the empty sacs as a Trojan horse to enter the cell stealthily.
This could allow viruses to establish a low-level infection in beta cells that’s hard to clear.
If further research confirms this proposed model, it could lead to the development of specific treatments to stop the virus infecting the beta cells, and prevent people from developing type 1 diabetes.
What’s the next step?
In their paper, the researchers note that previous work supports their idea, and that this area “deserves further study”.
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