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Fetal Brain Infection Is Not a Unique Characteristic of Brazilian Zika Viruses

Setoh YX 1 , Peng NY 2 , Nakayama E 3 , Amarilla AA 4 , Prow NA 5 , Suhrbier A 6 Show all authors , Khromykh AA 7

Affiliations 

  • 1 Australian Infectious Diseases Research Centre, School of Chemistry and Molecular Biosciences, The University of Queensland, St. Lucia 4072, Australia. y.setoh@uq.edu.au
  • 2 Australian Infectious Diseases Research Centre, School of Chemistry and Molecular Biosciences, The University of Queensland, St. Lucia 4072, Australia. y.g.peng@uq.net.au
  • 3 Inflammation Biology Group, QIMR Berghofer Medical Research Institute, Brisbane 4006, Australia. Eri.Nakayama@qimrberghofer.edu.au
  • 4 Australian Infectious Diseases Research Centre, School of Chemistry and Molecular Biosciences, The University of Queensland, St. Lucia 4072, Australia. a.amarillaortiz@uq.edu.au
  • 5 Inflammation Biology Group, QIMR Berghofer Medical Research Institute, Brisbane 4006, Australia. Natalie.Prow@qimrberghofer.edu.au
  • 6 Inflammation Biology Group, QIMR Berghofer Medical Research Institute, Brisbane 4006, Australia. andreas.suhrbier@qimrberghofer.edu.au
  • 7 Australian Infectious Diseases Research Centre, School of Chemistry and Molecular Biosciences, The University of Queensland, St. Lucia 4072, Australia. alexander.khromykh@uq.edu.au
Viruses, 2018 10 03;10(10).
PMID: 30282919 DOI: 10.3390/v10100541

Abstract

The recent emergence of Zika virus (ZIKV) in Brazil was associated with an increased number of fetal brain infections that resulted in a spectrum of congenital neurological complications known as congenital Zika syndrome (CZS). Herein, we generated de novo from sequence data an early Asian lineage ZIKV isolate (ZIKV-MY; Malaysia, 1966) not associated with microcephaly and compared the in vitro replication kinetics and fetal brain infection in interferon α/β receptor 1 knockout (IFNAR1-/-) dams of this isolate and of a Brazilian isolate (ZIKV-Natal; Natal, 2015) unequivocally associated with microcephaly. The replication efficiencies of ZIKV-MY and ZIKV-Natal in A549 and Vero cells were similar, while ZIKV-MY replicated more efficiently in wild-type (WT) and IFNAR-/- mouse embryonic fibroblasts. Viremias in IFNAR1-/- dams were similar after infection with ZIKV-MY or ZIKV-Natal, and importantly, infection of fetal brains was also not significantly different. Thus, fetal brain infection does not appear to be a unique feature of Brazilian ZIKV isolates.

* Title and MeSH Headings from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.

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