Neurodevelopmental protein Musashi-1 interacts with the Zika genome and promotes viral replication
Copyright policy )Neurodevelopmental protein Musashi-1 interacts with the Zika genome and promotes viral replication
Inherited microcephaly exposes Zika culprit Microcephaly has been the terrifying hallmark of the recent outbreak of Zika virus (ZIKV) in the Americas. How the virus damages brain development in the fetus is enigmatic. Chavali et al. found that in congenital microcephaly, mutations in a neural precursor protein, Musashi-1 (MSI1), impede RNA binding to neural stem cell targets, resulting in abnormal brain development (see the Perspective by Griffin). MSI1 also binds ZIKV RNA to amplify viral replication in cells. This interaction could put a pregnant woman at risk of giving birth to a microcephalic child. Furthermore, MSI1 is expressed at high levels in the mouse testis, which may explain the sexual transmission of this virus. Science , this issue p. 83 ; see also p. 33
- University of Leeds United Kingdom
- University of Cambridge United Kingdom
- Cambridge University Hospitals NHS Foundation Trust United Kingdom
- Radboud University Nijmegen Netherlands
- Centre for Life United Kingdom
Male, Zika Virus Infection, Brain, RNA-Binding Proteins, Radboudumc 9: Rare cancers RIHS: Radboud Institute for Health Sciences, Nerve Tissue Proteins, Genome, Viral, Zika Virus, Virus Replication, HEK293 Cells, Neural Stem Cells, Chlorocebus aethiops, Mutation, Microcephaly, Animals, Humans, Human Genetics - Radboud University Medical Center, Female, Child, Vero Cells
Male, Zika Virus Infection, Brain, RNA-Binding Proteins, Radboudumc 9: Rare cancers RIHS: Radboud Institute for Health Sciences, Nerve Tissue Proteins, Genome, Viral, Zika Virus, Virus Replication, HEK293 Cells, Neural Stem Cells, Chlorocebus aethiops, Mutation, Microcephaly, Animals, Humans, Human Genetics - Radboud University Medical Center, Female, Child, Vero Cells
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