Cambridge scientists uncover key protein in Zika virus pathology


The recent Zika virus outbreak has had a devastating global impact on human health, with at least 70 countries reporting infections since 2015.1 Zika virus is spread to humans by mosquito bites, although it can also be passed from person to person via sexual contact or bodily fluids, and from mother to foetus via the placenta. In children and adults, the virus causes only a mild illness. However, in pregnant women it can have devastating consequences for foetal neurodevelopment.

In the Americas, over the past two years, more than 3,500 babies have been confirmed to have congenital malformations associated with Zika virus infection.2 Perhaps the most tragic consequence of Zika virus on the unborn baby is microcephaly; a serious birth defect where the brain fails to develop properly, characterised by an abnormally small head.

Until recently, it was not known how the Zika virus caused neonatal microcephaly. However, scientists at the University of Cambridge have provided an insight into the mechanism by which the Zika virus may ‘hijack’ neural stem cells to cause this devastating brain condition.3 Their research showed that, in order to replicate, the Zika virus interacts with a neural stem cell protein called Musashi-1. In developing embryos, Musashi-1 is an RNA-binding protein that binds to target genes to regulate neural stem cell function. The interaction between the Zika virus and Musashi-1 disrupts this process and damages the foetal neural stem cells. Ultimately, neural stem cells die and the brain fails to develop to normal size.

Although, transmission of Zika virus may finally be slowing down, in the Americas at least,4 we are starting to understand the way that Zika virus causes microcephaly, giving scientists hope that, someday, we may be able to treat this devastating disease.

1. European Centre for Disease Prevention and Control. Rapid risk assessment: Zika virus epidemic, tenth update. 4 April 2017.

2. Pan American Health Organization/World Health Organization. Zika cases and congenital syndrome associated with Zika virus reported by countries and territories in the Americas, 2015–2017. 21 September 2017. www.paho.org/hq/index.php?option=com_content&view=article&id=12390&Itemid=42090. [Accessed September 2017]

3. Chavali PL, Stojic L, Meredith LW, et al. Neurodevelopmental protein Musashi-1 interacts with the Zika genome and promotes viral replication. Science 2017; 57 (6346): 83–88.

4. Pan American Health Organization/World Health Organization. Regional Zika Epidemiological Update (Americas) August 25, 2017. www.paho.org/hq/index.php?option=com_content&view=article&id=11599%3Aregional-zika-epidemiological-update-americas. [Accessed September 2017]

Ciara Whitty

Ciara Whitty  PhD

Editorial Project Manager

Oct 2017