ArticleThe American journal of pathology2003
Pathogenesis of Ebola hemorrhagic fever in cynomolgus macaques: evidence that dendritic cells are early and sustained targets of infection.
Article in The American journal of pathology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 337 papers, 2 of them syntheses that pooled it.
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Who cites it
337 citing papers in PubMed, 2 syntheses or guidelines pooled it, 568 citations in OpenAlex.
- A systematic review of the immuno-inflammatory dysfunction secondary to viral hemorrhagic fevers; Ebola and Lassa fever.PLoS neglected tropical diseases · 2025Pooled it
- Use of Ebola Vaccine: Recommendations of the Advisory Committee on Immunization Practices, United States, 2020.MMWR. Recommendations and reports : Morbidity and mortality weekly report. Recommendations and reports · 2021Guideline
- Differential glycosylation in the envelope glycoprotein enhances DC-SIGN-mediated cell entry of the West African Ebolavirus Makona.Emerging microbes & infections · 2026Article
- Self-adjuvanting Ebola virus-like particles that incorporate a cellular interferon-inducing domain.Research square · 2026Article
- Article
- Ebola virus disease in the modern era: pathogenesis, therapeutic advances, vaccine strategies, and global health preparedness.Infection · 2026Review
- Comparison of Ebola virus infection routes and resulting disease in animal models.Journal of virology · 2026Review
- Progression of nipah virus infection in the African green monkey: Role of macrophages and dendritic cells in early virus spread.iScience · 2026Article
- Recombinant Bombali ebolavirus in cynomolgus macaques as a survival model of Ebola virus disease.Nature communications · 2026Article
- Potential Mechanisms Underlying Bleeding During Infection With Hemorrhagic Fever Viruses.Arteriosclerosis, thrombosis, and vascular biology · 2026Review
- Ebola virus matrix protein VP40 triggers inflammatory responses linked to the ebolavirus virulence.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Delayed type I interferon response and the subsequent out-of-sequence cytokine signal inhibit T cell induction in non-surviving Ebola virus-infected patients.Frontiers in immunology · 2026Article
- 25 Years of Ebola Virus VP35 Research.Journal of molecular biology · 2025Review
- Ebola's hidden front: Neurological involvement and pathogenesis.PLoS pathogens · 2025Article
- Review
- Emerging and reemerging infectious diseases: global trends and new strategies for their prevention and control.Signal transduction and targeted therapy · 2024Review
- N-Substituted Pyrrole-Based Heterocycles as Broad-Spectrum Filoviral Entry Inhibitors.Journal of medicinal chemistry · 2024Article
- Rhabdomyolysis, Acute Kidney Injury, and Mortality in Ebola Virus Disease: Retrospective Analysis of Cases From the Eastern Democratic Republic of the Congo, 2019.The Journal of infectious diseases · 2024Article
- Vascular dysfunction in hemorrhagic viral fevers: opportunities for organotypic modeling.Biofabrication · 2024Review
- Ebola virus disease in children: epidemiology, pathogenesis, management, and prevention.Pediatric research · 2024Review
277 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ebola virus (EBOV) infection causes a severe and fatal hemorrhagic disease that in many ways appears to be similar in humans and nonhuman primates; however, little is known about the development of EBOV hemorrhagic fever. In the present study, 21 cynomolgus monkeys were experimentally infected with EBOV and examined sequentially over a 6-day period to investigate the pathological events of EBOV infection that lead to death. Importantly, dendritic cells in lymphoid tissues were identified as early and sustained targets of EBOV, implicating their important role in the immunosuppression characteristic of EBOV infections. Bystander lymphocyte apoptosis, previously described in end-stage tissues, occurred early in the disease-course in intravascular and extravascular locations. Of note, apoptosis and loss of NK cells was a prominent finding, suggesting the importance of innate immunity in determining the fate of the host. Analysis of peripheral blood mononuclear cell gene expression showed temporal increases in tumor necrosis factor-related apoptosis-inducing ligand and Fas transcripts, revealing a possible mechanism for the observed bystander apoptosis, while up-regulation of NAIP and cIAP2 mRNA suggest that EBOV has evolved additional mechanisms to resist host defenses by inducing protective transcripts in cells that it infects. The sequence of pathogenetic events identified in this study should provide new targets for rational prophylactic and chemotherapeutic interventions.
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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.