Researchers have made a “significant breakthrough” in understanding how a family of viruses including the winter-vomiting bug, norovirus, work.

The new study, led by the University of Glasgow, reveals the inner workings of the calicivirus family, which includes norovirus and sapoviruses – highly infectious viruses that can cause outbreaks of diarrhoea and vomiting.

Read more: What is norovirus and how to avoid it

It is hoped the research may provide a new target for the development of antiviral drugs to prevent diseases like norovirus, better known as the ‘winter-vomiting’ bug because incidence tends to peak in the coldest months.

Norovirus is highly contagious and can be very difficult to contain. Commonly outbreaks occur in crowded facilities like hospitals, care homes, schools, hotels and on cruise ships.

NHS Tayside were forced to close a ward in Strathcathro Hospital to new admissions at Christmas following several cases of vomiting and diarrhoea thought to be caused by norovirus.

In 2012, the luxury Gleneagles hotel was at the centre of one of Scotland’s most high profile norovirus outbreaks when more than 100 guests and members of staff were sickened with the bug, which can be fatal in people with weakened immune systems.

Read more: Norovirus outbreak leads to cancelled operations

There are currently no treatments available for norovirus, which can be spread person-to-person or through contaminated food. Shellfish can also carry the bug.

Caliciviruses are also important animal pathogens, causing ‘cat flu’ that can be associated with very high mortality rates in domestic cats.

Researchers at Glasgow University’s Centre for Virus Research used the Nobel prize-winning technique of Cryo-Electron Microscopy (CryoEM) to analyse the structure of the virus that causes ‘cat flu’ - feline calicivirus.

They discovered that after binding to the cell surface, these viruses undergo structural changes leading to the formation of a portal – a funnel-shaped structure on the virus particle surface – which is thought to insert into the membrane of the cell, allowing the virus to inject its genome into the host cell and begin the infection process.

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This insight into the early stages of calicivirus infection provides a new target for the development of antiviral drugs to prevent this family of viruses.

Dr David Bhella, who led the research, said: “We have made a significant break-through in understanding how this family of viruses initiate infections.

"When viruses infect us, they bind to and then enter our cells.

"This is often by a process known as ‘endocytosis’, the process cells use to bring in nutrients from their environment.”

Viruses trigger endocytosis, causing the cell to bring the virus particle (or virion) into the cell in a bubble or vesicle called an ‘endosome’.

The virus then needs to break out of the endosome to release their genes into the cell and start the infection.

Dr Bhella continued: “Furthermore, we have calculated an atomic model of the portal protein - known as VP2.

"While VP2 was known to be critical for the production of infectious virus, its function has been hitherto undetermined.

“Our finding that VP2 assembles a portal that is likely responsible for endosome escape represents a major step forward in our understanding of both the Caliciviridae and icosahedral RNA containing viruses in general.”

The research has been published in the journal, Nature.