ArticleCell reports2017
Crimean-Congo Hemorrhagic Fever Virus Suppresses Innate Immune Responses via a Ubiquitin and ISG15 Specific Protease.
Article in Cell reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 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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Who cites it
71 citing papers in PubMed, 96 citations in OpenAlex.
- Pathogenicity and virulence of Crimean-Congo hemorrhagic fever virus: From enzootic maintenance to severe human disease.Virulence · 2026Review
- Structures of the Crimean-Congo hemorrhagic fever virus RNA-dependent RNA polymerase.Cell discovery · 2026Article
- Structure-Guided Discovery and Biochemical Validation of Novel Small-Molecule Inhibitors Predicted to Target the CCHFV OTU Protease Y89-W99 Pocket.International journal of molecular sciences · 2026Article
- Nairobi sheep disease virus: an emerging threat with unresolved pathogenesis and zoonotic potential.Journal of virology · 2026Review
- Functional Characterization of OTU Domain-Containing Deubiquitinases from Plant Pathogenic Fungi Reveals Distinct Immune Modulatory Mechanisms.Journal of fungi (Basel, Switzerland) · 2026Article
- Article
- Skin Deep: Uncovering the Early Events of Crimean-Congo Hemorrhagic Fever Virus at the Tick-Host-Virus Interface.Viruses · 2026Review
- Review
- ISG15-USP18 signaling restrains viperin-dependent metabolic antiviral restriction.bioRxiv : the preprint server for biology · 2026Article
- Venturing into host-pathogen interaction in Crimean-Congo hemorrhagic fever to highlight terra incognita.Frontiers in immunology · 2026Review
- Crimean-Congo hemorrhagic fever virus NSm protein inhibits the type I interferon signaling by binding to STAT2.PLoS neglected tropical diseases · 2025Article
- Elevated interferon-induced transmembrane protein 3 in platelets and megakaryocytes suppresses Crimean-Congo hemorrhagic fever viral infection by interacting with glycoprotein Gc.Virologica Sinica · 2025Article
- Characteristics of viral ovarian tumor domain protease from two emerging orthonairoviruses and identification of Yezo virus human infections in northeastern China as early as 2012.Journal of virology · 2025Article
- A multiplex method for rapidly identifying viral protease inhibitors.Molecular systems biology · 2025Article
- Reverse Genetics System for Crimean-Congo Hemorrhagic Fever Virus.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Review
- The Role of Nucleocapsid Protein (NP) in the Immunology of Crimean-Congo Hemorrhagic Fever Virus (CCHFV).Viruses · 2024Review
- HuR (ELAVL1) regulates the CCHFV minigenome and HAZV replication by associating with viral genomic RNA.PLoS neglected tropical diseases · 2024Article
- Crimean Congo hemorrhagic fever virus nucleoprotein and GP38 subunit vaccine combination prevents morbidity in mice.NPJ vaccines · 2024Article
- Evaluation of two inoculation routes of an adenovirus-mediated viral protein inhibitor in a Crimean-Congo hemorrhagic fever mouse model.Virus research · 2024Article
11 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Antiviral responses are regulated by conjugation of ubiquitin (Ub) and interferon-stimulated gene 15 (ISG15) to proteins. Certain classes of viruses encode Ub- or ISG15-specific proteases belonging to the ovarian tumor (OTU) superfamily. Their activity is thought to suppress cellular immune responses, but studies demonstrating the function of viral OTU proteases during infection are lacking. Crimean-Congo hemorrhagic fever virus (CCHFV, family Nairoviridae) is a highly pathogenic human virus that encodes an OTU with both deubiquitinase and deISGylase activity as part of the viral RNA polymerase. We investigated CCHFV OTU function by inactivating protease catalytic activity or by selectively disrupting its deubiquitinase and deISGylase activity using reverse genetics. CCHFV OTU inactivation blocked viral replication independently of its RNA polymerase activity, while deubiquitinase activity proved critical for suppressing the interferon responses. Our findings provide insights into viral OTU functions and support the development of therapeutics and vaccines.
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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.