ArticleAntiviral research2018
Favipiravir (T-705) but not ribavirin is effective against two distinct strains of Crimean-Congo hemorrhagic fever virus in mice.
Article in Antiviral research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 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
47 citing papers in PubMed, 83 citations in OpenAlex.
- 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
- Identification of cellular ion channels that facilitate Hazara nairovirus infection enables selection of clinically approved compounds with anti-nairoviral properties.Scientific reports · 2026Article
- Review
- Inhibitory effects of molnupiravir on Crimean-Congo hemorrhagic fever virus polymerase.NAR molecular medicine · 2026Article
- Oral VV261 administration protects mice from lethal Crimean-Congo hemorrhagic fever virus challenge.Journal of virology · 2025Article
- Pathogenesis of Hazara orthonairovirus infection in type I interferon receptor-deficient mice and resolution of disease following 4'-fluorouridine therapy.Journal of virology · 2025Article
- Targeting the Rift Valley Fever Virus Polymerase: Resistance Mechanisms and Structural Insights.ACS infectious diseases · 2025Article
- A comprehensive overview of the burden, prevention, and therapeutic aspects of arboviral diseases in India.Communications medicine · 2025Review
- Article
- 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
- The Role of Nucleocapsid Protein (NP) in the Immunology of Crimean-Congo Hemorrhagic Fever Virus (CCHFV).Viruses · 2024Review
- Emerging and reemerging infectious diseases: global trends and new strategies for their prevention and control.Signal transduction and targeted therapy · 2024Review
- A replicating RNA vaccine confers protection in a rhesus macaque model of Crimean-Congo hemorrhagic fever.NPJ vaccines · 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
- Nucleocapsid protein-specific monoclonal antibodies protect mice against Crimean-Congo hemorrhagic fever virus.Nature communications · 2024Article
- Neutralizing monoclonal antibodies against the Gc fusion loop region of Crimean-Congo hemorrhagic fever virus.PLoS pathogens · 2024Article
- Crimean-Congo haemorrhagic fever (CCHF): present and future therapeutic armamentarium.Le infezioni in medicina · 2024Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
Crimean-Congo hemorrhagic fever virus (CCHFV) is a cause of serious hemorrhagic disease in humans. Humans infected with CCHFV develop a non-specific febrile illness and then progress to the hemorrhagic phase where case fatality rates can be as high as 30%. Currently there is lack of vaccines and the recommended antiviral treatment, ribavirin, has inconsistent efficacy in both human and animal studies. In this study we developed a model of CCHFV infection in type I interferon deficient mice using the clinical CCHFV isolate strain Hoti. Mice infected with strain Hoti develop a progressively worsening and ultimately fatal disease. We utilized this model along with our established model using the prototypical CCHFV strain 10200 to evaluate treatment with ribavirin or the antiviral favipiravir. While ribavirin treatment was able to suppress viral loads at early time points it was ultimately unable to prevent development of terminal disease in mice infected with either strain of CCHFV. In contrast, favipiravir showed clinical benefit even when administered late in the clinical progression of CCHF. Interestingly, in a small subset of mice, late-onset of CCHF was observed after favipiravir treatment was stopped and persistence of viral RNA in favipiravir treated survivors was also seen. Nevertheless, favipiravir showed significant clinical benefit against two distinct strains of CCHFV suggesting it may be a potent antiviral for treatment of human CCHFV infections.
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