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. 2019 Jan 18;15(1):e1007507. doi: 10.1371/journal.ppat.1007507

Fig 13. Summary diagram depicting potential mechanisms via which ZIKV may lead to fetal brain pathology in primates.

Fig 13

(A) In the normally developing primate cortex, radial glial (RG) fibers serve as scaffolding for migrating neurons and intermediate precursors (IP) to the CP [55]. During the second half of gestation, RG end-feet detach from the ventricular and pial surfaces removing the RG fiber scaffolding after the cortex has formed its layers [56–59]. During the second half of gestation, RG also gradually differentiate to astrocytes and pre-oligodendrocytes [57–61] with normal transformation to astrocytes in the fetal frontal cortex. Based on the present study and studies in macaques (33,34,37,38), ZIKV infection of the fetal cortex results in a loss in RG fibers (B) resulting in disorganized neuroprogenitor cells (C; intermediate precursors (IP) and migrating neurons). (D) The widely reported astrogliosis may be the result of premature differentiation of RG to astrocytes, and/or as part of the noted neuroinflammatory response to ZIKV that includes increased microglia and IL-6 (E). (F) ZIKV infection impacts developing oligodendrocytes leading to reduced myelination as observed in the pigtail macaque and as reported in human fetuses [37, 38]. (Abbreviations: VZ: ventricular zone; SVZ: subventricular zone; IZ: intermediate zone; SP: subplate; CP: cortical plate; MZ: marginal zone).