ArticlePLoS pathogens2024
c-FLIP facilitates ZIKV infection by mediating caspase-8/3-dependent apoptosis.
Article in PLoS pathogens, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Advances and applications of brain organoids in central nervous system disorders: Bridging the gap from laboratory to clinic.Neural regeneration research · 2026Article
- Zika virus: unraveling the complex interplay between viral pathogenesis and host immune defenses.Virology journal · 2026Review
- Review
- Mouse models of Zika virus infection-induced placenta and fetal brain damage.Journal of animal science · 2026Review
- Zika virus and host innate immunity: mechanisms of activation and evasion.Frontiers in immunology · 2026Review
- Nuclear respiratory factor-1 promotes CFLAR transcription in H9C2 cardiomyocytes, protecting them against hypoxia-induced apoptosis.Molecular biology reports · 2025Article
- Exploring the Causal Effects of Micronutrient Supplementation on Susceptibility to Viral Pneumonia: A Mendelian Randomization Study.Pathogens (Basel, Switzerland) · 2025Article
- RNA-Seq Reveals Transcriptome Changes Following Zika Virus Infection in Fetal Brains inViruses · 2024Article
Corrections and comments
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Authors and funding
19 authors.
Funding
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Abstract
c-FLIP functions as a dual regulator of apoptosis and inflammation, yet its implications in Zika virus (ZIKV) infection remain partially understood, especially in the context of ZIKV-induced congenital Zika syndrome (CZS) where both apoptosis and inflammation play pivotal roles. Our findings demonstrate that c-FLIP promotes ZIKV infection in placental cells and myeloid-derived macrophages, involving inflammation and caspase-8/3-mediated apoptosis. Moreover, our observations reveal that c-FLIP augments ZIKV infection in multiple tissues, including blood cell, spleen, uterus, testis, and the brain of mice. Notably, the partial deficiency of c-FLIP provides protection to embryos against ZIKV-induced CZS, accompanied by a reduction in caspase-3-mediated apoptosis. Additionally, we have found a distinctive parental effect of c-FLIP influencing ZIKV replication in fetal heads. In summary, our study reveals the critical role of c-FLIP as a positive regulator in caspase-8/3-mediated apoptosis during ZIKV infection, significantly contributing to the development of CZS.
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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 Socratic graph.