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Modelling Zika Virus Infection of the Developing Human Brain In Vitro Using Stem Cell Derived Cerebral Organoids
Published on: September 19, 2017
Zika virus infection histories in brain development
Bruna L M Marcelino1, Brendha L Dos Santos2, Jhulimar G Doerl1,3
1Brain Institute, Federal University of Rio Grande do Norte, 59056-450 Natal, Brazil.
Abstract:
An outbreak of births of microcephalic patients in Brazil motivated multiple studies on this incident. The data left no doubt that infection by Zika virus (ZIKV) was the cause, and that this virus promotes reduction in neuron numbers and neuronal death. Analysis of patients' characteristics revealed additional aspects of the pathology alongside the decrease in neuronal number. Here, we review the data from human, molecular, cell and animal model studies attempting to build the natural history of ZIKV in the embryonic central nervous system (CNS). We discuss how identifying the timing of infection and the pathways through which ZIKV may infect and spread through the CNS can help explain the diversity of phenotypes found in congenital ZIKV syndrome (CZVS). We suggest that intraneuronal viral transport is the primary mechanism of ZIKV spread in the embryonic brain and is responsible for most cases of CZVS. According to this hypothesis, the viral transport through the blood-brain barrier and cerebrospinal fluid is responsible for more severe pathologies in which ZIKV-induced malformations occur along the entire anteroposterior CNS axis.
Insights
Zika virus (ZIKV) causes congenital ZIKV syndrome (CZVS), leading to reduced neuron numbers and death. Intracellular transport is the main ZIKV spread mechanism in the embryonic brain, explaining diverse CZVS phenotypes.
Area of Science:
- Neuroscience
- Virology
- Developmental Biology
Background:
- The Zika virus (ZIKV) outbreak in Brazil highlighted its teratogenic effects, specifically microcephaly.
- ZIKV infection in utero causes significant reduction in neuron numbers and neuronal death in the developing central nervous system (CNS).
Approach:
- This review synthesizes data from human, molecular, cellular, and animal model studies.
- It focuses on understanding the natural history of ZIKV within the embryonic CNS.
- The study examines the timing and pathways of ZIKV infection and spread.
Key Points:
- Intraneuronal viral transport is proposed as the primary mechanism for ZIKV spread within the embryonic brain.
- This mechanism is linked to the majority of congenital ZIKV syndrome (CZVS) cases.
- Viral transport across the blood-brain barrier and cerebrospinal fluid may cause more severe ZIKV-induced CNS malformations.
Conclusions:
- Understanding ZIKV's embryonic CNS infection dynamics is crucial for explaining CZVS phenotypic diversity.
- Intraneuronal transport is key to ZIKV pathogenesis in the developing brain.
- Further research into viral spread pathways can inform strategies to mitigate severe congenital malformations.
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