The sight of newborn infants with radically reduced brain sizes (microcephaly) has seized attention worldwide and thrust the Zika virus into the limelight as the probable culprit. Zika spreads through mosquito bites and belongs to the Flaviviridae virus family, but how does Zika infection cause such devastating abnormalities in developing infants?
A multidisciplinary team led by Hengli Tang, Hongjun Song, and Guo-li Ming set out to answer this question and have published their results in a recent Cell Stem Cell study. The effects on the brain led the authors to study potentially detrimental effects of Zika virus infection on neural progenitors which give rise to the brain’s cerebral cortex.
This line of thinking soon hit pay dirt, as they found that:
- Zika virus passaged in monkey and mosquito cells infected human cells at varying efficiencies
- They found low-efficiency infection of human embryonic kidney cells (HEK293), human embryonic stem cells (hESCs), and human induced pluripotent stem cells (hiPSCs)
- However, Zika did infect hiPSC-derived embryonic cortical neural progenitors (hNPCs) at high efficiency
- Zika-infected hNPCs produced and released infectious Zika virus
- Zika infection increased Caspase-3 activity and promoted hNPC death
- Zika infection also significantly altered the expression of various cell cycle regulator genes and genes involved in protein transport and localization in hNPCs
The data presented suggest that Zika may infect and either kill or prohibit developing neural progenitors from functioning properly, and so lead to the abnormalities observed in newborn children. The authors hope that their “tractable experimental model system” can be put to good use as an investigative tool, but also as a means to screen for compounds that can inhibit the effect of Zika virus infection.
Check out the science behind all the newspaper headlines at Cell Stem Cell, March 2016.