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Nat Microbiol. 2018 Oct;3(10):1161-1174. doi: 10.1038/s41564-018-0236-1. Epub 2018 Sep 10.

Male offspring born to mildly ZIKV-infected mice are at risk of developing neurocognitive disorders in adulthood.

Author information

1
Heinrich Pette Institute, Leibniz Institute for Experimental Virology, Hamburg, Germany.
2
Neuronal Development, Center for Molecular Neurobiology Hamburg (ZNMH), University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
3
Research Group for Behavioral Biology, Center for Molecular Neurobiology Hamburg (ZNMH), University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
4
Department of Pathology, University of Veterinary Medicine, Hannover, Germany.
5
Center of Systems Neuroscience, Hannover, Germany.
6
Department of Pharmacology, Toxicology and Pharmacy, University of Veterinary Medicine, Hannover, Germany.
7
Department of Infectious Diseases, Molecular Virology, Heidelberg University, Heidelberg, Germany.
8
Bernhard Nocht Institute for Tropical Medicine, Hamburg, Germany.
9
German Centre for Infection Research (DZIF), Partner Site Hamburg-Lübeck-Borstel-Riems, Hamburg, Germany.
10
Institute of Neuroimmunology and Multiple Sclerosis, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
11
Department of Diagnostic and Interventional Radiology and Nuclear Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
12
Department of Ophthalmology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
13
Institute for Clinical and Laboratory Chemistry, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
14
Department of Obstetrics and Fetal Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
15
University of Helsinki and Helsinki University Hospital, Helsinki, Finland.
16
Tropical Pathology and Infectious Disease Association, Cusco, Peru.
17
Institute of Developmental Genetics, Helmholtz Zentrum München, Neuherberg, Germany.
18
German Mouse Clinic, Institute of Experimental Genetics, Helmholtz Zentrum München, Neuherberg, Germany.
19
Chair of Experimental Genetics, School of Life Science Weihenstephan, Technical University of Munich, Freising, Germany.
20
German Center for Diabetes Research (DZD), Neuherberg, Germany.
21
Heinrich Pette Institute, Leibniz Institute for Experimental Virology, Hamburg, Germany. guelsah.gabriel@leibniz-hpi.de.
22
German Centre for Infection Research (DZIF), Partner Site Hamburg-Lübeck-Borstel-Riems, Hamburg, Germany. guelsah.gabriel@leibniz-hpi.de.
23
Center for Structural and Cell Biology in Medicine, University of Lübeck, Lübeck, Germany. guelsah.gabriel@leibniz-hpi.de.
24
University of Veterinary Medicine, Hannover, Germany. guelsah.gabriel@leibniz-hpi.de.

Abstract

Congenital Zika virus (ZIKV) syndrome may cause fetal microcephaly in ~1% of affected newborns. Here, we investigate whether the majority of clinically inapparent newborns might suffer from long-term health impairments not readily visible at birth. Infection of immunocompetent pregnant mice with high-dose ZIKV caused severe offspring phenotypes, such as fetal death, as expected. By contrast, low-dose (LD) maternal ZIKV infection resulted in reduced fetal birth weight but no other obvious phenotypes. Male offspring born to LD ZIKV-infected mothers had increased testosterone (TST) levels and were less likely to survive in utero infection compared to their female littermates. Males also presented an increased number of immature neurons in apical and basal hippocampal dendrites, while female offspring had immature neurons in basal dendrites only. Moreover, male offspring with high but not very high (storm) TST levels were more likely to suffer from learning and memory impairments compared to females. Future studies are required to understand the impact of TST on neuropathological and neurocognitive impairments in later life. In summary, increased sex-specific vigilance is required in countries with high ZIKV prevalence, where impaired neurodevelopment may be camouflaged by a healthy appearance at birth.

PMID:
30202017
DOI:
10.1038/s41564-018-0236-1

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