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Epidemiological studies show that in utero fetal infection with the Zika virus (ZIKV) may lead to microcephaly, an irreversible congenital malformation of the brain characterized by an incomplete development of the cerebral cortex. However, the mechanism of Zika virus-associated microcephaly remains unclear.
Combined analysis of human fetuses infected with Zika virus, cultures of human neuronal stem cells and mice embryos showed that ZIKV infection of cortical progenitors -stem cells for cortical neurons) controlling neurogenesis triggers stress in the endoplasmic reticulum -where some of the cellular proteins and lipids are synthesized in the embryonic brain, inducing signals in response to incorrect protein conformation.
When it reaches the brain, Zika virus infects neuronal stem cells, which will generate fewer neurons, and by inducing chronic stress in the endoplasmic reticulum, it promotes apoptosis-the early death of these neuronal cells. These two combined mechanisms explain why the cerebral cortex of infected fetuses becomes deficient in neurons and is therefore smaller in size.
Researchers administered an inhibitors of protein-folding re-sponse in cortical progenitors and found that this inhibited the development of microcephaly in mice embryos infected with Zika virus. The defects observed are specific to an infection by ZIKV, as other neurotropical viruses of the flavivirus family- West Nile virus and yellow fever did not cause microcephaly, in contrast to Zika virus.
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