The Zika virus diverts a key protein necessary for creating new brain cells in the developing human foetus, causing the birth defect microcephaly in which babies are born with abnormally small brains, a new study has found.

The findings also suggest that Zika virus may be susceptible to existing antiviral drugs that could prevent disruption to the developing nervous system, said the researchers.

Scientists at Yale University in the US showed that Zika virus kills stem cells in the brain and disrupts the process of creating new brain cells.

An analysis shows that the virus diverts a form of the protein TBK1 from its primary job of organising cell division to the mitochondria, the cell’s power house, where it helps initiate an immune response.

Lacking the protein at the site of cell division, cells die instead of forming new brain cells, resulting in microcephaly.

The data suggest this mechanism may also contribute to microcephaly associated with other common congenital viral infections.

Researchers found that an existing drug, Sofosbuvir, showed promise in preventing Zika virus infection of neural stem cells in laboratory culture and also seems to keep phospho-TBK1 involved in cell division.

More study needs to be conducted to prove the efficacy of the drug as a medical therapy for Zika virus, researchers said.

"There is an urgent need to identify therapeutic approaches to halt Zika infection, especially in pregnant women," said Marco Onorati, researcher in the lab of Nenad Sestan, professor at Yale.

"In the interim, we hope these findings can lead to therapies that might minimise the damage caused by this virus."

The research was published in the journal Cell Reports.