ReviewInternational journal of biological sciences2023
Targeting Type I Interferon Induction and Signaling: How Zika Virus Escapes from Host Innate Immunity.
Review in International journal of biological sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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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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
15 citing papers in PubMed, 21 citations in OpenAlex.
- PTBP1 is upregulated in response to Zika virus infection and restrains viral replication by hijacking viral NS1 protein to induce NS1 degradation.Journal of virology · 2026Article
- Peripheral blood mononuclear cell gene expression signatures predict long-term survivorship in canine DLBCL.Scientific reports · 2026Article
- Article
- Zinc finger protein ZNF33B facilitates Japanese encephalitis virus replication by regulating mCell & bioscience · 2026Article
- Zika virus and host innate immunity: mechanisms of activation and evasion.Frontiers in immunology · 2026Review
- Interplay between flaviviruses and the interferon response: mechanisms of immune evasion and therapeutic implications.Frontiers in pharmacology · 2026Review
- Comparison of human cerebral organoids infected with wild-type Zika versus attenuated DN-2 virus strains uncovers differences in host immune responses.Cell communication and signaling : CCS · 2025Article
- Zika virus and the fetal-maternal interface: deciphering the mechanisms of placental infection and implications for pregnancy outcomes.Emerging microbes & infections · 2025Review
- Review
- Robust antiviral innate immune response and miRNA regulatory network were identified in ZIKV-infected cells: implications in the pathogenesis of ZIKV infection.Virus genes · 2025Article
- From "immune silence" to "immune dialogue": modification strategies for bone substitutes based on bone immunomodulatory characteristics.Frontiers in cell and developmental biology · 2025Review
- The inoculum dose of Zika virus can affect the viral replication dynamics, cytokine responses and survival rate in immunocompromised AG129 mice.Molecular biomedicine · 2024Article
- The NS1 protein of contemporary West African Zika virus potentiates viral replication and reduces innate immune activation.PLoS neglected tropical diseases · 2024Article
- Extracellular Vesicles inInternational journal of molecular sciences · 2024Review
- Evaluation of Genes and Molecular Pathways Common between Diffuse Large B-cell Lymphoma (DLBCL) and Systemic Lupus Erythematosus (SLE): A Systems Biology Approach.Medical journal of the Islamic Republic of Iran · 2024Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Zika virus (ZIKV) infection causes neurological disorders and draws great attention. ZIKV infection can elicit a wide range of immune response. Type I interferons (IFNs) as well as its signaling cascade play crucial role in innate immunity against ZIKV infection and in turn ZIKV can antagonize them. ZIKV genome are mainly recognized by Toll-like receptors 3 (TLR3), TLR7/8 and RIG-I-like receptor 1 (RIG-1), which induces the expression of Type I IFNs and interferon-stimulated genes (ISGs). ISGs exert antiviral activity at different stages of the ZIKV life cycle. On the other hand, ZIKV takes multiple strategies to antagonize the Type Ⅰ IFN induction and its signaling pathway to establish a pathogenic infection, especially by using the viral nonstructural (NS) proteins. Most of the NS proteins can directly interact with the factors in the pathways to escape the innate immunity. In addition, structural proteins also participate in the innate immune evasion and activation of antibody-binding of blood dendritic cell antigen 2 (BDCA2) or inflammasome also be used to enhance ZIKV replication. In this review, we summarize the recent findings about the interaction between ZIKV infection and type I IFNs pathways and suggest potential strategies for antiviral drug development.
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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.