Format

Send to

Choose Destination
Cell Microbiol. 2017 Jun;19(6). doi: 10.1111/cmi.12744. Epub 2017 May 3.

Zika infection and the development of neurological defects.

Author information

1
Department of Surgery, University of São Paulo, São Paulo, Brazil.
2
Department of Microbiology, University of São Paulo, São Paulo, Brazil.
3
Department of Pathology, University of Pernambuco, Recife, Pernambuco, Brazil.
4
Department of Obstetrics, School of Arts Sciences and Humanities, São Paulo, Brazil.

Abstract

Starting with the outbreak in Brazil, Zika virus (ZIKV) infection has been correlated with severe syndromes such as congenital Zika syndrome and Guillain-Barré syndrome. Here, we review the status of Zika virus pathogenesis in the central nervous system (CNS). One of the main concerns about ZIKV exposure during pregnancy is abnormal brain development, which results in microcephaly in newborns. Recent advances in in vitro research show that ZIKV can infect and obliterate cells from the CNS, such as progenitors, neurons, and glial cells. Neural progenitor cells seem to be the main target of the virus, with infection leading to less cell migration, neurogenesis impairment, cell death and, consequently, microcephaly in newborns. The downsizing of the brain can be directly associated with defective development of the cortical layer. In addition, in vivo investigations in mice reveal that ZIKV can cross the placenta and migrate to fetuses, but with a significant neurotropism, which results in brain damage for the pups. Another finding shows that hydrocephaly is an additional consequence of ZIKV infection, being detected during embryonic and fetal development in mouse, as well as after birth in humans. In spite of the advances in ZIKV research in the last year, the mechanisms underlying ZIKV infection in the CNS require further investigation particularly as there are currently no treatments or vaccines against ZIKV infection.

KEYWORDS:

ZIKV; Zika; brain damage; congenital Zika syndrome; flaviviruses; microcephaly

PMID:
28370966
DOI:
10.1111/cmi.12744
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Wiley
Loading ...
Support Center