Zika virus [ZV] infection in pregnancy causes microcephaly in the developing fetus. The cause and effect relationship is well established through human case studies and experimental models. The fetal neural tissue development is markedly disrupted by the ZV with the most significant effect on the developing grey matter of the brain tissue via the infection of neural progenitor cells and widespread apoptosis. ZV infects undifferentiated precursor neuronal cells that are rapidly undergoing mitosis, thus making it highly likely to perturb mitotic spindle and centromere related genes and proteins. The infected cells fail to differentiate into functional neurons and undergo apoptosis. Reviewing the literature informs that ZV infects the undifferentiated neural stem cells and the cells expressing the AXL receptors. The focused gene expression studies in ZV infected cells may help to identify the perturbed genes and the mechanisms of apoptosis of the selected cell population as well as the pathology of microcephaly itself.
The purpose of this review is to understand the most vulnerable cell type susceptible to ZV infection in context with the changes in human ZV-induced microcephalic brain tissue morphology, mouse model and in vitro spheroids and organoids studies. Here we discuss the human brain development and correlate it with the experimental evidence of the ZV effects on the neuronal development in vivo and in vitro.
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