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1 Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
2 Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA. Electronic address: piersontc@mail.nih.gov.
1 Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
2 Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA. Electronic address: piersontc@mail.nih.gov.
The current Zika virus (ZIKV) outbreak is associated with high numbers of human congenital birth defects, yet it has been unclear how ZIKV infection during pregnancy causes these abnormalities. Three new mouse models now show that ZIKV crosses the placenta and replicates in the brains of fetal mice.
Figure 1. Current Murine Models for ZIKV-Induced Fetal Abnormalities
Left panel) ICR fetuses carefully injected…
Figure 1. Current Murine Models for ZIKV-Induced Fetal Abnormalities
Left panel) ICR fetuses carefully injected intracerebrally exhibit viral infection of the brain and reduced brain size by 5 days post-infection. Middle panel) SJL mice infected with a Brazilian ZIKV isolate give birth to pups with whole-body growth delay and IUGR. Viral replication can be detected in fetal brains. Right panel) After ZIKV-infection of IFNAR−/− dams carrying IFNAR+/− heterozygous fetuses, the virus replicates in placental trophoblasts and neurons. Most fetuses undergo demise and resorption, while surviving fetuses exhibit IUGR.
Miner JJ, Cao B, Govero J, Smith AM, Fernandez E, Cabrera OH, Garber C, Noll M, Klein RS, Noguchi KK, Mysorekar IU, Diamond MS.Miner JJ, et al.Cell. 2016 May 19;165(5):1081-1091. doi: 10.1016/j.cell.2016.05.008. Epub 2016 May 11.Cell. 2016.PMID: 27180225Free PMC article.
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