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Ann Neurol. 2017 Jul;82(1):121-127. doi: 10.1002/ana.24968.

Differential neuronal susceptibility and apoptosis in congenital Zika virus infection.

Author information

1
Department of Pathology, University of Maryland School of Medicine, Baltimore, MD.
2
Division of Pathology, Children's National Health System, Washington, DC.
3
Department of Pathology, Johns Hopkins Medical Institutions, Baltimore, MD.
4
Department of Diagnostic Radiology and Imaging, Children's National Health System, Washington, DC.
5
Center for Neuroscience Research, Children's National Health System, Washington, DC.
6
Department of Pediatrics, School of Medicine and Health Sciences, George Washington University, Washington, DC.
7
Pharmacology and Physiology, School of Medicine and Health Sciences, George Washington University, Washington, DC.
8
Fetal Medicine Institute, Children's National Health System, Washington, DC.
9
Division of Pediatric Infectious Diseases, Children's National Health System, Washington, DC.
10
Microbiology, Immunology, and Tropical Medicine, School of Medicine and Health Sciences, George Washington University, Washington, DC.

Abstract

To characterize the mechanism of Zika virus (ZIKV)-associated microcephaly, we performed immunolabeling on brain tissue from a 20-week fetus with intrauterine ZIKV infection. Although 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. Ann Neurol 2017;82:121-127.

PMID:
28556287
DOI:
10.1002/ana.24968
[Indexed for MEDLINE]

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