ZIKV can infect human term placentas in the absence of maternal factors

Zika virus infection can result in devastating pregnancy outcomes when it crosses the placental barrier. For human pregnancies, the mechanisms of vertical transmission remain enigmatic. Utilizing a human placenta-cotyledon perfusion model, we examined Zika virus exposure in the absence of maternal f...

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Published inCommunications biology Vol. 5; no. 1; p. 243
Main Authors Villazana-Kretzer, Diana L., Wuertz, Kathryn McGuckin, Newhouse, Daniel, Damicis, Jennifer R., Dornisch, Elisabeth M., Voss, Kathleen M., Muruato, Antonio E., Paymaster, Jennifer A., Schmiedecke, Stacey S., Edwards, Sarah M., Napolitano, Peter G., Tisoncik-Go, Jennifer, Ieronimakis, Nicholas, Gale, Michael
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 18.03.2022
Nature Publishing Group
Nature Portfolio
Subjects
13/21
13/51
14/1
14/19
14/63
38/39
38/90
631/250/254
692/699/255/2514
96/2
Apoptosis
Biology
Biomedical and Life Sciences
Cell death
Cotyledons
Female
Gene expression
Humans
Immune response
Infections
Infectious Disease Transmission, Vertical
Innate immunity
Life Sciences
Perfusion
Placenta
Pregnancy
Pregnancy Complications, Infectious - pathology
Transcription factors
Viral infections
Viruses
Zika virus
Zika Virus - physiology
Zika Virus Infection
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Abstract Zika virus infection can result in devastating pregnancy outcomes when it crosses the placental barrier. For human pregnancies, the mechanisms of vertical transmission remain enigmatic. Utilizing a human placenta-cotyledon perfusion model, we examined Zika virus exposure in the absence of maternal factors. To distinguish responses related to viral infection vs . recognition, we evaluated cotyledons perfused with either active or inactivated Zika virus. Active Zika virus exposure resulted in infection, cell death and syncytium injury. Pathology corresponded with transcriptional changes related to inflammation and innate immunity. Inactive Zika virus exposure also led to syncytium injury and related changes in gene expression but not cell death. Our observations reveal pathologies and innate immune responses that are dependent on infection or virus placenta interactions independent of productive infection. Importantly, our findings indicate that Zika virus can infect and compromise placentas in the absence of maternal humoral factors that may be protective. Villazana-Kretzer et al. compare histology, physiology and gene expression in cotyledons from term placentas perfused with either active or UV-inactivated Zika virus. They show that ZIKV can infect human term placentas in the absence of maternal factors and identify unique transcriptional responses to active ZIKA virus.
AbstractList Zika virus infection can result in devastating pregnancy outcomes when it crosses the placental barrier. For human pregnancies, the mechanisms of vertical transmission remain enigmatic. Utilizing a human placenta-cotyledon perfusion model, we examined Zika virus exposure in the absence of maternal factors. To distinguish responses related to viral infection vs. recognition, we evaluated cotyledons perfused with either active or inactivated Zika virus. Active Zika virus exposure resulted in infection, cell death and syncytium injury. Pathology corresponded with transcriptional changes related to inflammation and innate immunity. Inactive Zika virus exposure also led to syncytium injury and related changes in gene expression but not cell death. Our observations reveal pathologies and innate immune responses that are dependent on infection or virus placenta interactions independent of productive infection. Importantly, our findings indicate that Zika virus can infect and compromise placentas in the absence of maternal humoral factors that may be protective.Villazana-Kretzer et al. compare histology, physiology and gene expression in cotyledons from term placentas perfused with either active or UV-inactivated Zika virus. They show that ZIKV can infect human term placentas in the absence of maternal factors and identify unique transcriptional responses to active ZIKA virus.
Villazana-Kretzer et al. compare histology, physiology and gene expression in cotyledons from term placentas perfused with either active or UV-inactivated Zika virus. They show that ZIKV can infect human term placentas in the absence of maternal factors and identify unique transcriptional responses to active ZIKA virus.
Abstract Zika virus infection can result in devastating pregnancy outcomes when it crosses the placental barrier. For human pregnancies, the mechanisms of vertical transmission remain enigmatic. Utilizing a human placenta-cotyledon perfusion model, we examined Zika virus exposure in the absence of maternal factors. To distinguish responses related to viral infection vs . recognition, we evaluated cotyledons perfused with either active or inactivated Zika virus. Active Zika virus exposure resulted in infection, cell death and syncytium injury. Pathology corresponded with transcriptional changes related to inflammation and innate immunity. Inactive Zika virus exposure also led to syncytium injury and related changes in gene expression but not cell death. Our observations reveal pathologies and innate immune responses that are dependent on infection or virus placenta interactions independent of productive infection. Importantly, our findings indicate that Zika virus can infect and compromise placentas in the absence of maternal humoral factors that may be protective.
Zika virus infection can result in devastating pregnancy outcomes when it crosses the placental barrier. For human pregnancies, the mechanisms of vertical transmission remain enigmatic. Utilizing a human placenta-cotyledon perfusion model, we examined Zika virus exposure in the absence of maternal factors. To distinguish responses related to viral infection vs. recognition, we evaluated cotyledons perfused with either active or inactivated Zika virus. Active Zika virus exposure resulted in infection, cell death and syncytium injury. Pathology corresponded with transcriptional changes related to inflammation and innate immunity. Inactive Zika virus exposure also led to syncytium injury and related changes in gene expression but not cell death. Our observations reveal pathologies and innate immune responses that are dependent on infection or virus placenta interactions independent of productive infection. Importantly, our findings indicate that Zika virus can infect and compromise placentas in the absence of maternal humoral factors that may be protective.
Zika virus infection can result in devastating pregnancy outcomes when it crosses the placental barrier. For human pregnancies, the mechanisms of vertical transmission remain enigmatic. Utilizing a human placenta-cotyledon perfusion model, we examined Zika virus exposure in the absence of maternal factors. To distinguish responses related to viral infection vs . recognition, we evaluated cotyledons perfused with either active or inactivated Zika virus. Active Zika virus exposure resulted in infection, cell death and syncytium injury. Pathology corresponded with transcriptional changes related to inflammation and innate immunity. Inactive Zika virus exposure also led to syncytium injury and related changes in gene expression but not cell death. Our observations reveal pathologies and innate immune responses that are dependent on infection or virus placenta interactions independent of productive infection. Importantly, our findings indicate that Zika virus can infect and compromise placentas in the absence of maternal humoral factors that may be protective. Villazana-Kretzer et al. compare histology, physiology and gene expression in cotyledons from term placentas perfused with either active or UV-inactivated Zika virus. They show that ZIKV can infect human term placentas in the absence of maternal factors and identify unique transcriptional responses to active ZIKA virus.
ArticleNumber 243
Author Voss, Kathleen M.
Ieronimakis, Nicholas
Wuertz, Kathryn McGuckin
Villazana-Kretzer, Diana L.
Muruato, Antonio E.
Dornisch, Elisabeth M.
Paymaster, Jennifer A.
Gale, Michael
Napolitano, Peter G.
Damicis, Jennifer R.
Newhouse, Daniel
Edwards, Sarah M.
Schmiedecke, Stacey S.
Tisoncik-Go, Jennifer
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crossref_primary_10_3390_pathogens13070555
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Snippet Zika virus infection can result in devastating pregnancy outcomes when it crosses the placental barrier. For human pregnancies, the mechanisms of vertical...
Abstract Zika virus infection can result in devastating pregnancy outcomes when it crosses the placental barrier. For human pregnancies, the mechanisms of...
Villazana-Kretzer et al. compare histology, physiology and gene expression in cotyledons from term placentas perfused with either active or UV-inactivated Zika...
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SubjectTerms 13/21
13/51
14/1
14/19
14/63
38/39
38/90
631/250/254
692/699/255/2514
96/2
Apoptosis
Biology
Biomedical and Life Sciences
Cell death
Cotyledons
Female
Gene expression
Humans
Immune response
Infections
Infectious Disease Transmission, Vertical
Innate immunity
Life Sciences
Perfusion
Placenta
Pregnancy
Pregnancy Complications, Infectious - pathology
Transcription factors
Viral infections
Viruses
Zika virus
Zika Virus - physiology
Zika Virus Infection
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Title ZIKV can infect human term placentas in the absence of maternal factors
URI https://link.springer.com/article/10.1038/s42003-022-03158-6
https://www.ncbi.nlm.nih.gov/pubmed/35304593
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https://pubmed.ncbi.nlm.nih.gov/PMC8933440
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