ArticleViruses2018
Human Fetal Astrocytes Infected with Zika Virus Exhibit Delayed Apoptosis and Resistance to Interferon: Implications for Persistence.
Article in Viruses, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
40 citing papers in PubMed, 77 citations in OpenAlex.
- Aedes aegypti salivary gland extract enhances Zika virus replication through immune modulation.Memorias do Instituto Oswaldo Cruz · 2026Article
- The human neural cell atlas of Zika virus infection in developing brain tissue.Cell reports. Medicine · 2025Article
- Neural and endothelial cell-derived extracellular vesicles mediate Zika virus genome dissemination and productive infection in vivo.PloS one · 2025Article
- Epidemic Zika virus strains from the Asian lineage induce an attenuated fetal brain pathogenicity.Nature communications · 2024Article
- A zebrafish-based in vivo model of Zika virus infection unveils alterations of the glutamatergic neuronal development and NS4A as a key viral determinant of neuropathogenesis.PLoS pathogens · 2024Article
- Distinct Replication Kinetics, Cytopathogenicity, and Immune Gene Regulation in Human Microglia Cells Infected with Asian and African Lineages of Zika Virus.Microorganisms · 2024Article
- Zika Virus Neuropathogenesis-Research and Understanding.Pathogens (Basel, Switzerland) · 2024Review
- Role of inflammatory cytokine burst in neuro-invasion of Japanese Encephalitis virus infection: an immunotherapeutic approaches.Journal of neurovirology · 2024Review
- Exploring Zika Virus Impact on Endothelial Permeability: Insights into Transcytosis Mechanisms and Vascular Leakage.Viruses · 2024Review
- Zika Virus: A Neurotropic Warrior against High-Grade Gliomas-Unveiling Its Potential for Oncolytic Virotherapy.Viruses · 2024Review
- Article
- Neurotoxic properties of the Zika virus envelope protein.Experimental neurology · 2023Article
- Mechanisms of Zika astrocyte infection and neuronal toxicity.NeuroImmune pharmacology and therapeutics · 2023Article
- Immune Functions of Astrocytes in Viral Neuroinfections.International journal of molecular sciences · 2023Review
- Astrocytes derived from neural progenitor cells are susceptible to Zika virus infection.PloS one · 2023Article
- Exploring epigenetic reprogramming during central nervous system infection.Immunological reviews · 2022Review
- Article
- Intrinsic features of Zika Virus non-structural proteins NS2A and NS4A in the regulation of viral replication.PLoS neglected tropical diseases · 2022Article
- Apoptosis during ZIKA Virus Infection: Too Soon or Too Late?International journal of molecular sciences · 2022Review
- Astrocyte Control of Zika Infection Is Independent of Interferon Type I and Type III Expression.Biology · 2022Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
Abstract
Zika virus (ZIKV) infection and persistence during pregnancy can lead to microcephaly and other fetal neurological disorders collectively known as Congenital Zika Syndrome. The immunological and virological events that contribute to the establishment of persistent ZIKV infection in humans are unclear though. Here we show that human fetal astrocytes (HFAs), the most abundant cell type in the central nervous system, become persistently infected with ZIKV resulting in continuous viral shedding for at least one month; a process that is facilitated by TIM/TAM receptors. HFAs are relatively resistant to ZIKV-induced apoptosis, a factor that may be important for chronic infection of these cells. Once infection was established, interferon treatment did not reduce virus replication. Moreover, the fact that the innate immune system was highly activated in persistently infected HFAs indicates that the virus can thrive in the presence of a sustained antiviral response. RNAseq analyses of persistently infected cells revealed that ZIKV alters host gene expression in a manner that could affect developmental processes. Conversely, data from sequencing of ZIKV genomes in persistently infected HFAs suggest that adaptive mutations were not required for establishing chronic infection. Based on these results, we postulate that HFAs are reservoirs for ZIKV in the fetal brain and that moderate apoptosis combined with inefficient antiviral response from these cells may contribute to the establishment of chronic brain infection associated with the ZIKV neurodevelopmental abnormalities.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.