Zika virus has been propelled onto a global stage because of its ability to infect the developing fetus and cause congenital abnormalities in brain development. While preventing Zika virus infection is an important goal of research on the virus, we hope to use the virus as a model for understanding embryonic brain development.
Development of the brain proceeds through a number of stages in which progenitors divide and migrate in the developing cortex. The birth defect microcephaly involves a reduction in the division of neurons which leads to a smaller brain. Such a condition may be caused by mutation or an infectious agent.
Mice are often used to study brain development, and its susceptibility to Zika virus infection allows us to use this virus to not only understand the basis of microcephaly and other brain disorders, but also provide information on how the brain develops. In the coming months we plan to infect mouse embryos with Zika virus and document the effect of infection on the different stages of brain development. An example is provided by the image, which shows the normal cytoarchitecture of the developing mouse brain at embryonic day 15. By using antibodies against viral and cellular proteins, we can assess the affect of Zika virus infection on migrating neurons (red), and a protein (Tbr1) required for neuronal migration (white).
The study of viruses has always provided insight into cell functions, and Zika virus is no exception.