ArticlePloS one2018
Zika virus as an oncolytic treatment of human neuroblastoma cells requires CD24.
Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 2 of them syntheses that pooled it.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
22 citing papers in PubMed, 2 syntheses or guidelines pooled it, 43 citations in OpenAlex.
- Pooled it
- Zika virus and brain cancer: Can Zika be an effective treatment for brain cancer? A systematic review.Oncotarget · 2024Pooled it
- Multi-omics analysis reveals key immunogenic signatures induced by oncolytic Zika virus infection of paediatric brain tumour cells.Scientific reports · 2025Article
- SMAC mimetics sensitize HIV-infected cells to oncolytic virus-mediated death.Frontiers in immunology · 2025Article
- Article
- The Oncolytic Activity of Zika Viral Therapy in Human Neuroblastoma In Vivo Models Confers a Major Survival Advantage in a CD24-dependent Manner.Cancer research communications · 2024Article
- Flaviviruses in AntiTumor Therapy.Viruses · 2023Review
- Higher replication potential of West Nile virus governs apoptosis induction in human neuroblastoma cells.Apoptosis : an international journal on programmed cell death · 2023Article
- Integrated re-analysis of transcriptomic and proteomic datasets reveals potential mechanisms for Zika viral-based oncolytic therapy in neuroblastoma.F1000Research · 2023Article
- The power of mumps virus: Matrix protein activates apoptotic pathways in human colorectal cell lines.PloS one · 2023Article
- Surprising magic of CD24 beyond cancer.Frontiers in immunology · 2023Review
- Article
- Apoptosis during ZIKA Virus Infection: Too Soon or Too Late?International journal of molecular sciences · 2022Review
- Immunovirotherapy for Pediatric Solid Tumors: A Promising Treatment That is Becoming a Reality.Frontiers in immunology · 2022Review
- Progress of oncolytic virotherapy for neuroblastoma.Frontiers in pediatrics · 2022Review
- AXL receptor is required for Zika virus strain MR-766 infection in human glioblastoma cell lines.Molecular therapy oncolytics · 2021Article
- The liver X receptor agonist LXR 623 restricts flavivirus replication.Emerging microbes & infections · 2021Article
- Characterization of Pathogenesis and Inflammatory Responses to Experimental Parechovirus Encephalitis.Frontiers in immunology · 2021Article
- The Propagation and Quantification of Two Emerging Oncolytic Viruses: Vesicular Stomatitis (VSV) and Zika (ZIKV).Methods in molecular biology (Clifton, N.J.) · 2020Article
- Downregulation of microRNA-3934-5p induces apoptosis and inhibits the proliferation of neuroblastoma cells by targeting TP53INP1.Experimental and therapeutic medicine · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neuroblastoma is the second most common childhood tumor. Survival is poor even with intensive therapy. In a search for therapies to neuroblastoma, we assessed the oncolytic potential of Zika virus. Zika virus is an emerging mosquito-borne pathogen unique among flaviviruses because of its association with congenital defects. Recent studies have shown that neuronal progenitor cells are likely the human target of Zika virus. Neuroblastoma has been shown to be responsive to infection. In this study, we show that neuroblastoma cells are widely permissive to Zika infection, revealing extensive cytopathic effects (CPE) and producing high titers of virus. However, a single cell line appeared poorly responsive to infection, producing undetectable levels of non-structural protein 1 (NS1), limited CPE, and low virus titers. A comparison of these poorly permissive cells to highly permissive neuroblastoma cells revealed a dramatic loss in the expression of the cell surface glycoprotein CD24 in poorly permissive cells. Complementation of CD24 expression in these cells led to the production of detectable levels of NS1 expression after infection with Zika, as well as dramatic increases in viral titers and CPE. Complementary studies using the Zika virus index strain and a north African isolate confirmed these phenotypes. These results suggest a possible role for CD24 in host cell specificity by Zika virus and offer a potential therapeutic target for its treatment. In addition, Zika viral therapy can serve as an adjunctive treatment for neuroblastoma by targeting tumor cells that can lead to recurrent disease and treatment failure.
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Registered trials
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.