ArticlePathogens & immunity2017
Jak Inhibitors Modulate Production of Replication-Competent Zika Virus in Human Hofbauer, Trophoblasts, and Neuroblastoma cells.
Article in Pathogens & immunity, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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The trial behind it
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Who cites it
20 citing papers in PubMed, 27 citations in OpenAlex.
- Yellow Fever in Pregnancy: A Comprehensive Review of the Clinical Implications and Vaccination in the Context of the 2024-2026 Americas Outbreak.Tropical medicine and infectious disease · 2026Review
- ZIKV envelope protein is a strong blocker of early directional differentiation in the neural lineage.Communications biology · 2026Article
- Vertical Transmission of Zika Virus: The Immune-Pathophysiological Interface of the Placenta.Journal of immunology research · 2026Review
- JAK inhibitors remove innate immune barriers facilitating viral propagation.NAR molecular medicine · 2025Article
- Immune Recognition versus Immune Evasion Systems in Zika Virus Infection.Biomedicines · 2023Review
- Interferon alpha and beta receptor 1 knockout in human embryonic kidney 293 cells enhances the production efficiency of proteins or adenoviral vectors related to type I interferons.Frontiers in bioengineering and biotechnology · 2023Article
- Anti-inflammatory compounds reduce equine herpesvirus type 1 replication and cell-to-cell spread.Frontiers in veterinary science · 2023Article
- An overview of Zika virus genotypes and their infectivity.Revista da Sociedade Brasileira de Medicina Tropical · 2022Review
- Type I interferon receptor (Frontiers in immunology · 2022Article
- Placental Macrophage (Hofbauer Cell) Responses to Infection During Pregnancy: A Systematic Scoping Review.Frontiers in immunology · 2021Article
- Targeting Macrophage Dysregulation for Viral Infections: Novel Targets for Immunomodulators.Frontiers in immunology · 2021Review
- The potential of JAK/STAT pathway inhibition by ruxolitinib in the treatment of COVID-19.Cytokine & growth factor reviews · 2020Review
- Article
- Synthesis of 4'-Substituted-2'-Deoxy-2'-α-Fluoro Nucleoside Analogs as Potential Antiviral Agents.Molecules (Basel, Switzerland) · 2020Article
- Pre- and peri-implantation Zika virus infection impairs fetal development by targeting trophectoderm cells.Nature communications · 2019Article
- Clinical Importance of Placental Testing among Suspected Cases of Congenital Zika Syndrome.International journal of molecular sciences · 2019Article
- An Update on Sexual Transmission of Zika Virus.Pathogens (Basel, Switzerland) · 2018Review
- Experimental Zika Virus Infection in the Pregnant Common Marmoset Induces Spontaneous Fetal Loss and Neurodevelopmental Abnormalities.Scientific reports · 2018Article
- Hofbauer Cells: Their Role in Healthy and Complicated Pregnancy.Frontiers in immunology · 2018Review
- Zika in the Americas, year 2: What have we learned? What gaps remain? A report from the Global Virus Network.Antiviral research · 2017Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Zika Virus (ZIKV) is a flavivirus that has been implicated in causing brain deformations, birth defects, and microcephaly in fetuses, and associated with Guillain-Barre syndrome. Mechanisms responsible for transmission of ZIKV across the placenta to the fetus are incompletely understood. Herein, we define key events modulating infection in clinically relevant cells, including primary placental macrophages (human Hofbauer cells; HC), trophoblasts, and neuroblastoma cells. Consistent with previous findings, HC and trophoblasts are permissive to ZIKV infection. Decrease of interferon signaling by Jak ½ inhibition (using ruxolitinib) significantly increased ZIKV replication in HC, trophoblasts, and neuroblasts. Enhanced ZIKV production in ruxolitinib-treated HC was associated with increased expression of HLA-DR and DC-SIGN. Nucleoside analogs blocked ruxolitinib-mediated production of extracellular virus. Although low-level ZIKV infection occurred in untreated HC and trophoblasts, replicating virions were incapable of infecting naive Vero cells. These deficient virions from untreated HC have "thin-coats" suggesting an immature structure. Blocking Jak ½ signaling (with ruxolitinib) restored replication competence as virions produced under these conditions confer cytopathic effects to naive Vero cells. These data demonstrate that Jak-STAT signaling directly impacts the ability of primary placental cells to produce replication-competent virus and is a key determinant in the production of mature virions in clinically relevant cells, including HC and trophoblasts. Design of targeted agents to prevent ZIKV replication in the placenta should consider Jak ½ signaling, the impact of its block on ZIKV infection, and subsequent transmission to the fetus.
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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.