ArticleJournal of virology2018
Exploring Crimean-Congo Hemorrhagic Fever Virus-Induced Hepatic Injury Using Antibody-Mediated Type I Interferon Blockade in Mice.
Article in Journal of virology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 76 citations in OpenAlex.
- Pathogenicity and virulence of Crimean-Congo hemorrhagic fever virus: From enzootic maintenance to severe human disease.Virulence · 2026Review
- Modulating Chikungunya and Mayaro virus-induced disease severity in mice using low concentrations of anti-IFNAR1 antibodies.Emerging microbes & infections · 2026Article
- Loss of type I interferon signaling in Kupffer cells triggers viral spread and fatal liver damage in a mouse model of Crimean-Congo hemorrhagic fever.PLoS pathogens · 2026Article
- Side-by-side evaluation of two Crimean-Congo hemorrhagic fever virus isolates in IFNARNpj viruses · 2026Article
- Article
- Review
- Pathogenicity of a novel orthonairovirus, Iwanai Valley virus, in mice.The Journal of veterinary medical science · 2026Article
- Microbiological perspectives on Crimean-Congo hemorrhagic fever: Seroprevalence and viral pathogenesis in Iraq.Biotechnology notes (Amsterdam, Netherlands) · 2026Article
- Venturing into host-pathogen interaction in Crimean-Congo hemorrhagic fever to highlight terra incognita.Frontiers in immunology · 2026Review
- Inhibitory effects of molnupiravir on Crimean-Congo hemorrhagic fever virus polymerase.NAR molecular medicine · 2026Article
- 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
- Single dose VSV-based vaccine protects mice against lethal heterologous Crimean-Congo hemorrhagic fever virus challenge.NPJ vaccines · 2025Article
- Antibodies targeting Crimean-Congo hemorrhagic fever virus GP38 limit vascular leak and viral spread.Science translational medicine · 2025Article
- Inflammation associated with monocyte/macrophage activation and recruitment corresponds with lethal outcome in a mouse model of Crimean-Congo haemorrhagic feverEmerging microbes & infections · 2024Article
- Antibodies targeting the Crimean-Congo Hemorrhagic Fever Virus nucleoprotein protect via TRIM21.Nature communications · 2024Article
- Emerging and reemerging infectious diseases: global trends and new strategies for their prevention and control.Signal transduction and targeted therapy · 2024Review
- Evaluation of two inoculation routes of an adenovirus-mediated viral protein inhibitor in a Crimean-Congo hemorrhagic fever mouse model.Virus research · 2024Article
- Antibodies targeting Crimean-Congo hemorrhagic fever virus GP38 limit vascular leak and viral spread.bioRxiv : the preprint server for biology · 2024Article
- Third International Conference on Crimean-Congo Hemorrhagic Fever in Thessaloniki, Greece, September 19-21, 2023.Antiviral research · 2024Review
- Establishment of a lethal mouse model of emerging tick-borne orthonairovirus infections.PLoS pathogens · 2024Article
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Crimean-Congo hemorrhagic fever virus (CCHFV) can cause severe hepatic injury in humans. However, the mechanism(s) causing this damage is poorly characterized. CCHFV produces an acute disease, including liver damage, in mice lacking type I interferon (IFN-I) signaling due to either STAT-1 gene deletion or disruption of the IFN-I receptor 1 gene. Here, we explored CCHFV-induced liver pathogenesis in mice using an antibody to disrupt IFN-I signaling. When IFN-I blockade was induced within 24 h postexposure to CCHFV, mice developed severe disease with greater than 95% mortality by 6 days postexposure. In addition, we observed increased proinflammatory cytokines, chemoattractants, and liver enzymes in these mice. Extensive liver damage was evident by 4 days postexposure and was characterized by hepatocyte necrosis and the loss of CLEC4F-positive Kupffer cells. Similar experiments in CCHFV-exposed NOD-SCID-γ (NSG), Rag2-deficient, and perforin-deficient mice also demonstrated liver injury, suggesting that cytotoxic immune cells are dispensable for hepatic damage. Some apoptotic liver cells contained viral RNA, while other apoptotic liver cells were negative, suggesting that cell death occurred by both intrinsic and extrinsic mechanisms. Protein and transcriptional analysis of livers revealed that activation of tumor necrosis factor superfamily members occurred by day 4 postexposure, implicating these molecules as factors in liver cell death. These data provide insights into CCHFV-induced hepatic injury and demonstrate the utility of antibody-mediated IFN-I blockade in the study of CCHFV pathogenesis in mice.
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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.