ArticleNature communications2018
Discordant congenital Zika syndrome twins show differential in vitro viral susceptibility of neural progenitor cells.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 78 papers.
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Who cites it
78 citing papers in PubMed.
- Zika exposure during pregnancy and the risk of hospitalisation and death due to community-acquired pneumonia in early childhood: a nationwide registry-based cohort study in Brazil.Lancet regional health. Americas · 2026Article
- Co-Expression Network Analyses Reveal Long Non-Coding RNA Programs Associated with Trophoblast Development and Response to Zika Virus Infection in Twins Discordant for Congenital Zika Syndrome.International journal of molecular sciences · 2026Article
- West Nile virus and Zika virus infections induce aggresome formation in human neural progenitor and A549 cells.Journal of virology · 2026Article
- Interleukin-27 is antiviral against Zika virus at the maternal-fetal interface.Nature communications · 2025Article
- A Scoping Review of Genetic Risk Factors Possibly Impacting Virally Induced Brain Injury After Zika Infection.Pediatric research · 2025Article
- Zika Virus: A Tale of Two Lineages.Pathogens (Basel, Switzerland) · 2025Review
- Building a growing genomic repository for maternal and fetal health through the PING Consortium.Pediatric research · 2025Article
- Genetic variants underlying congenital Zika syndrome and severe microcephaly: a systematic review and meta-analysis.Virusdisease · 2025Article
- Multi-omics analysis reveals key immunogenic signatures induced by oncolytic Zika virus infection of paediatric brain tumour cells.Scientific reports · 2025Article
- Congenital Zika virus infection in laboratory animals: a comparative review highlights translational studies on the maternal-foetal interface.Memorias do Instituto Oswaldo Cruz · 2025Review
- Identification of natural Zika virus peptides presented on the surface of paediatric brain tumour cells by HLA class I.PloS one · 2025Article
- Zika virus vertical transmission induces neuroinflammation and synapse impairment in brain cells derived from children born with Congenital Zika Syndrome.Scientific reports · 2024Article
- Genetically modified ZIKA virus as a microRNA-sensitive oncolytic virus against central nervous system tumors.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- Zika Virus Infection Alters the Circadian Clock Expression in Human Neuronal Monolayer and Neurosphere Cultures.Cellular and molecular neurobiology · 2023Article
- Insights into Zika Virus Pathogenesis and Potential Therapeutic Strategies.Biomedicines · 2023Review
- ZIKV infection differentially affects the transcriptional profiles in HTR8 and U251 cells.Virus research · 2023Article
- Noncoding RNA of Zika Virus Affects Interplay between Wnt-Signaling and Pro-Apoptotic Pathways in the Developing Brain Tissue.Viruses · 2023Article
- Association between genetic variants in TREM1, CXCL10, IL4, CXCL8 and TLR7 genes with the occurrence of congenital Zika syndrome and severe microcephaly.Scientific reports · 2023Article
- Stem Cell Technology in Organ Transplantation: A Novel Method for 3D Bioprinting Functional and Stable Liver Grafts Using Human iPS Cells Derived Cells.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Recurrence of COVID-19 associated with reduced T-cell responses in a monozygotic twin pair.Open biology · 2022Article
18 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
42 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Congenital Zika syndrome (CZS) causes early brain development impairment by affecting neural progenitor cells (NPCs). Here, we analyze NPCs from three pairs of dizygotic twins discordant for CZS. We compare by RNA-Seq the NPCs derived from CZS-affected and CZS-unaffected twins. Prior to Zika virus (ZIKV) infection the NPCs from CZS babies show a significantly different gene expression signature of mTOR and Wnt pathway regulators, key to a neurodevelopmental program. Following ZIKV in vitro infection, cells from affected individuals have significantly higher ZIKV replication and reduced cell growth. Whole-exome analysis in 18 affected CZS babies as compared to 5 unaffected twins and 609 controls excludes a monogenic model to explain resistance or increased susceptibility to CZS development. Overall, our results indicate that CZS is not a stochastic event and depends on NPC intrinsic susceptibility, possibly related to oligogenic and/or epigenetic mechanisms.
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