Abstract
To characterize the mechanism of ZIKV-associated microcephaly, we perform immunolabeling on brain tissue from a 20-week fetus with intrauterine ZIKV infection. While ZIKV demonstrated a wide range of neuronal and non-neuronal tropism, the infection rate was highest in intermediate progenitor cells and immature neurons. Apoptosis was observed in both infected and uninfected bystander cortical neurons, suggesting a role for paracrine factors in induction of neuronal apoptosis. Our results highlight differential neuronal susceptibility and neuronal apoptosis as potential mechanisms in the development of ZIKV-associated microcephaly, and may provide insights into the design and best timing of future therapy. This article is protected by copyright. All rights reserved.
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