Abstract
ObjectivesEffects of Zika virus (ZIKV) infection on placental development during pregnancy are unclear.MethodsFull‐term placentas from three women, each infected with ZIKV during specific pregnancy trimesters, were harvested for anatomic, immunologic and transcriptomic analysis.ResultsIn this study, each woman exhibited a unique immune response with raised IL‐1RA, IP‐10, EGF and RANTES expression and neutrophil numbers during the acute infection phase. Although ZIKV NS3 antigens co‐localised to placental Hofbauer cells, the placentas showed no anatomic defects. Transcriptomic analysis of samples from the placentas revealed that infection during trimester 1 caused a disparate cellular response centred on differential eIF2 signalling, mitochondrial dysfunction and oxidative phosphorylation. Despite these, the babies were delivered without any congenital anomalies.ConclusionThese findings should translate to improve clinical prenatal screening procedures for virus‐infected pregnant patients.
Highlights
Zika virus (ZIKV) caused numerous outbreaks of infection worldwide,[1] and the scale of these outbreaks highlighted several features of ZIKV infection that had previously been unrecognised or under-reported
15% of Patient 1’s CD14+ monocytes were positive for ZIKV NS3 antigens, which persisted to a lesser degree in the convalescent phase (7.61%)
Patient 3 exhibited a ‘delayed’ infectious response, in which 2.66% of CD14+ monocytes were positive for ZIKV NS3 antigen levels during the acute phase, which increased to 10.1% of total CD14+ monocytes during the convalescent phase (Table 1 and Supplementary figure 1a, b)
Summary
Zika virus (ZIKV) caused numerous outbreaks of infection worldwide,[1] and the scale of these outbreaks highlighted several features of ZIKV infection that had previously been unrecognised or under-reported. One such feature included congenital foetal growth-associated anomalies as a result of ZIKV infection during pregnancy, termed congenital Zika syndrome (CZS).[2,3] Pregnancy is divided into three trimesters, based on the series of developmental changes that occur in the foetus and the physiological changes that occur in the mother. Understanding the nature of the ZIKV–host interactions at each trimester is required to determine the consequences of maternal–foetal ZIKV transmission. While the unique immunologic state experienced during pregnancy prevents the mother from rejecting the foetus,[5] the state of pregnancy could increase the mother’s susceptibility to infection.[6]
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