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Updated: Mar 1, 2026
Zika Virus Infectious Cell Culture System and the In Vitro Prophylactic Effect of Interferons
Published on: August 23, 2016
Neurodevelopmental protein Musashi-1 interacts with the Zika genome and promotes viral replication
Pavithra L Chavali1, Lovorka Stojic1, Luke W Meredith2
1Cancer Research UK Cambridge Institute, Li Ka Shing Centre, University of Cambridge, Robinson Way, Cambridge CB2 0RE, UK.
Abstract:
A recent outbreak of Zika virus in Brazil has led to a simultaneous increase in reports of neonatal microcephaly. Zika targets cerebral neural precursors, a cell population essential for cortical development, but the cause of this neurotropism remains obscure. Here we report that the neural RNA-binding protein Musashi-1 (MSI1) interacts with the Zika genome and enables viral replication. Zika infection disrupts the binding of MSI1 to its endogenous targets, thereby deregulating expression of factors implicated in neural stem cell function. We further show that MSI1 is highly expressed in neural progenitors of the human embryonic brain and is mutated in individuals with autosomal recessive primary microcephaly. Selective MSI1 expression in neural precursors could therefore explain the exceptional vulnerability of these cells to Zika infection.
Insights
Zika virus infection targets neural precursors by interacting with Musashi-1 (MSI1), a protein crucial for brain development. This interaction disrupts normal neural stem cell function, potentially explaining microcephaly during Zika outbreaks.
Area of Science:
- Neuroscience
- Virology
- Genetics
Background:
- Zika virus outbreak in Brazil linked to increased neonatal microcephaly.
- Zika virus neurotropism in cerebral neural precursors is not well understood.
Purpose of the Study:
- Investigate the mechanism of Zika virus neurotropism.
- Identify host factors involved in Zika virus replication and pathogenesis.
Main Methods:
- Studied the interaction between Zika virus genome and Musashi-1 (MSI1).
- Assessed the effect of Zika infection on MSI1 binding to endogenous targets.
- Examined MSI1 expression in human embryonic brain neural progenitors.
- Analyzed MSI1 mutations in individuals with autosomal recessive primary microcephaly.
Main Results:
- Musashi-1 (MSI1) interacts with the Zika virus genome, facilitating viral replication.
- Zika infection disrupts MSI1's binding to its normal targets, altering neural stem cell gene expression.
- MSI1 is highly expressed in human embryonic neural progenitors.
- MSI1 mutations are found in primary microcephaly cases.
Conclusions:
- Musashi-1 (MSI1) is a key host factor enabling Zika virus replication in neural precursors.
- Disruption of MSI1 function by Zika virus contributes to neurodevelopmental defects like microcephaly.
- Selective MSI1 expression in neural precursors explains their vulnerability to Zika infection.
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