TY - JOUR
T1 - Animal models of congenital zika syndrome provide mechanistic insight into viral pathogenesis during pregnancy
AU - Narasimhan, Harish
AU - Chudnovets, Anna
AU - Burd, Irina
AU - Pekosz, Andrew
AU - Klein, Sabra L.
N1 - Funding Information:
The writing of this review was funded by NIH/NICHD R01HD097608 (IB and SK). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. We thank Patrick Creisher and Morgan Sherer for edits and assistance with figure development.
Publisher Copyright:
© 2020 Narasimhan et al.
PY - 2020/10
Y1 - 2020/10
N2 - In utero Zika virus (ZIKV; family Flaviviridae) infection causes a distinct pattern of birth defects and disabilities in the developing fetus and neonate that has been termed congenital zika syndrome (CZS). Over 8,000 children were affected by the 2016 to 2017 ZIKV outbreak in the Americas, many of whom developed CZS as a result of in utero exposure. To date, there is no consensus about how ZIKV causes CZS; animal models, however, are providing mechanistic insights. Using nonhuman primates, immunocompromised mice, immunocompetent mice, and other animal models (e.g., pigs, sheep, guinea pigs, and hamsters), studies are showing that maternal immunological responses, placental infection and inflammation, as well as viral genetic factors play significant roles in predicting the downstream consequences of in utero ZIKV infection on the development of CZS in offspring. There are thousands of children suffer-ing from adverse consequences of CZS. Therefore, the animal models developed to study ZIKV-induced adverse outcomes in offspring could provide mechanistic insights into how other viruses, including influenza and hepatitis C viruses, impact placental viability and fetal growth to cause long-term adverse outcomes in an effort to identify therapeutic treatments.
AB - In utero Zika virus (ZIKV; family Flaviviridae) infection causes a distinct pattern of birth defects and disabilities in the developing fetus and neonate that has been termed congenital zika syndrome (CZS). Over 8,000 children were affected by the 2016 to 2017 ZIKV outbreak in the Americas, many of whom developed CZS as a result of in utero exposure. To date, there is no consensus about how ZIKV causes CZS; animal models, however, are providing mechanistic insights. Using nonhuman primates, immunocompromised mice, immunocompetent mice, and other animal models (e.g., pigs, sheep, guinea pigs, and hamsters), studies are showing that maternal immunological responses, placental infection and inflammation, as well as viral genetic factors play significant roles in predicting the downstream consequences of in utero ZIKV infection on the development of CZS in offspring. There are thousands of children suffer-ing from adverse consequences of CZS. Therefore, the animal models developed to study ZIKV-induced adverse outcomes in offspring could provide mechanistic insights into how other viruses, including influenza and hepatitis C viruses, impact placental viability and fetal growth to cause long-term adverse outcomes in an effort to identify therapeutic treatments.
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U2 - 10.1371/journal.pntd.0008707
DO - 10.1371/journal.pntd.0008707
M3 - Review article
C2 - 33091001
AN - SCOPUS:85094163938
SN - 1935-2727
VL - 14
SP - 1
EP - 20
JO - PLoS neglected tropical diseases
JF - PLoS neglected tropical diseases
IS - 10
M1 - e0008707
ER -