ArticleNature microbiology2024
Crimean-Congo haemorrhagic fever virus uses LDLR to bind and enter host cells.
Article in Nature microbiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
29 citing papers in PubMed, 38 citations in OpenAlex.
- The Crimean-Congo haemorrhagic fever virus hijacks the liver lipid metabolic pathway for virion production.Emerging microbes & infections · 2026Article
- Pathogenicity and virulence of Crimean-Congo hemorrhagic fever virus: From enzootic maintenance to severe human disease.Virulence · 2026Review
- CCHFV GP38 and GP85 interact with cell-surface glycosaminoglycans.Npj viruses · 2026Article
- Nairobi sheep disease virus: an emerging threat with unresolved pathogenesis and zoonotic potential.Journal of virology · 2026Review
- Human antibody targeting Crimean-Congo hemorrhagic fever virus glycoprotein 38 protects mice against heterologous virus challenge.The Journal of clinical investigation · 2026Article
- A non-canonical JAK/STAT pathway promotes viral replication through the lipoprotein receptor-related protein in ticks.PLoS biology · 2026Article
- Design of a neutralizing and protective pan-encephalitic alphavirus receptor decoy protein.Science translational medicine · 2026Article
- 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
- Repurposing Cilnidipine as an entry inhibitor against Crimean-Congo Hemorrhagic Fever pseudovirus infection.Archives of virology · 2026Article
- Venturing into host-pathogen interaction in Crimean-Congo hemorrhagic fever to highlight terra incognita.Frontiers in immunology · 2026Review
- Pathogenesis of Hazara orthonairovirus infection in type I interferon receptor-deficient mice and resolution of disease following 4'-fluorouridine therapy.Journal of virology · 2025Article
- LRP1 facilitates Jamestown Canyon virus infection of neurons.Journal of virology · 2025Article
- State-selective small molecule degraders that preferentially remove aggregates and oligomers.Nature communications · 2025Article
- Article
- Article
- Immunogenicity of NSDV GP38 and the role of furin in GP38 proteolytic processing.Journal of virology · 2025Article
- Harnessing Hazara Virus as a Surrogate for Crimean-Congo Hemorrhagic Fever Virus Enables Inactivation Studies at a Low Biosafety Level.Pathogens (Basel, Switzerland) · 2025Article
- Viral hijacking of host DDX60 promotes Crimean-Congo haemorrhagic fever virus replication via G-quadruplex unwinding.PLoS pathogens · 2025Article
Corrections and comments
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Authors and funding
28 authors at 9 institutions in 7 countries.
Funding
Abstract
Climate change and population densities accelerated transmission of highly pathogenic viruses to humans, including the Crimean-Congo haemorrhagic fever virus (CCHFV). Here we report that the Low Density Lipoprotein Receptor (LDLR) is a critical receptor for CCHFV cell entry, playing a vital role in CCHFV infection in cell culture and blood vessel organoids. The interaction between CCHFV and LDLR is highly specific, with other members of the LDLR protein family failing to bind to or neutralize the virus. Biosensor experiments demonstrate that LDLR specifically binds the surface glycoproteins of CCHFV. Importantly, mice lacking LDLR exhibit a delay in CCHFV-induced disease. Furthermore, we identified the presence of Apolipoprotein E (ApoE) on CCHFV particles. Our findings highlight the essential role of LDLR in CCHFV infection, irrespective of ApoE presence, when the virus is produced in tick cells. This discovery holds profound implications for the development of future therapies against CCHFV.
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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.