ArticleCell host & microbe2015
Flavivirus Antagonism of Type I Interferon Signaling Reveals Prolidase as a Regulator of IFNAR1 Surface Expression.
Article in Cell host & microbe, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 papers.
What it found
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Who cites it
93 citing papers in PubMed, 143 citations in OpenAlex.
- Type I interferon mitigates ZIKV-induced neuroinflammation and cell death in the central nervous system.Virus research · 2026Article
- Powassan Virus NS5 Antagonizes TYK2-Mediated Immune Signaling Pathways.bioRxiv : the preprint server for biology · 2026Article
- Virus-host interactome reveals host cellular pathways perturbed by tick-borne encephalitis virus infection.iScience · 2026Article
- Review
- Proviral NUP153 binding to viral proteins and RNA regulates structural-nonstructural protein ratios in orthoflavivirus infection.Nature communications · 2026Article
- Transcriptomic insights into the neuropathogenic and immune response alterations in mouse neurons challenged with west nile and japanese encephalitis viruses.Virology journal · 2026Article
- Mendelian Randomization and Single-Cell RNA Sequencing Reveal CKAP4 and PFDN5 as Tumor Cell-Specific Causal Genes for Glioblastoma.International journal of general medicine · 2026Article
- Interplay between flaviviruses and the interferon response: mechanisms of immune evasion and therapeutic implications.Frontiers in pharmacology · 2026Review
- Coevolutionary constraints of Zika virus nonstructural protein 5 replication and interferon antagonism activities.bioRxiv : the preprint server for biology · 2025Article
- Pathogenicity and virulence of Powassan virus.Virulence · 2025Review
- Viral interferon antagonism shapes host tropism.PLoS pathogens · 2025Review
- PIM1 Attenuates Innate Immunity to Foster Coronavirus Replication through Ubiquitin Ligase β-TrCP-Mediated IFNAR1 Degradation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Differences in biomarker levels and proteomic survival prediction across two COVID-19 cohorts with distinct treatments.iScience · 2025Article
- The segmented flavivirus Alongshan virus reduces mitochondrial mass by degrading STAT2 to suppress the innate immune response.Journal of virology · 2025Article
- Interferon-alpha/beta receptor deficiency enhances susceptibility to Powassan virus infection in mice.Frontiers in microbiology · 2025Article
- Zika virus NS5 protein inhibits type I interferon signaling via CRL3 E3 ubiquitin ligase-mediated degradation of STAT2.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- The Flavivirus Non-Structural Protein 5 (NS5): Structure, Functions, and Targeting for Development of Vaccines and Therapeutics.Vaccines · 2024Review
- Robust CXCL10/IP-10 and CCL5/RANTES Production Induced by Tick-Borne Encephalitis Virus in Human Brain Pericytes Despite Weak Infection.International journal of molecular sciences · 2024Article
- Evolution of STAT2 resistance to flavivirus NS5 occurred multiple times despite genetic constraints.Nature communications · 2024Article
- Lessons Learned from West Nile Virus Infection:Vaccinations in Equines and Their Implications for One Health Approaches.Viruses · 2024Review
33 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
23 authors at 9 institutions in 3 countries.
Funding
Abstract
Type I interferon (IFN-α/β or IFN-I) signals through two receptor subunits, IFNAR1 and IFNAR2, to orchestrate sterile and infectious immunity. Cellular pathways that regulate IFNAR1 are often targeted by viruses to suppress the antiviral effects of IFN-I. Here we report that encephalitic flaviviruses, including tick-borne encephalitis virus and West Nile virus, antagonize IFN-I signaling by inhibiting IFNAR1 surface expression. Loss of IFNAR1 was associated with binding of the viral IFN-I antagonist, NS5, to prolidase (PEPD), a cellular dipeptidase implicated in primary immune deficiencies in humans. Prolidase was required for IFNAR1 maturation and accumulation, activation of IFNβ-stimulated gene induction, and IFN-I-dependent viral control. Human fibroblasts derived from patients with genetic prolidase deficiency exhibited decreased IFNAR1 surface expression and reduced IFNβ-stimulated signaling. Thus, by understanding flavivirus IFN-I antagonism, prolidase is revealed as a central regulator of IFN-I responses.
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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.