ArticleJournal of virology2002
Hantavirus infection of dendritic cells.
Article in Journal of virology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
53 citing papers in PubMed, 135 citations in OpenAlex.
- β2 integrin mediates hantavirus-induced release of neutrophil extracellular traps.The Journal of experimental medicine · 2014Trial
- The role of immune cells in Hantaan-induced hemorrhagic fever with renal syndrome.Frontiers in immunology · 2026Review
- Hemorrhagic Fever with Renal Syndrome in Asia: History, Pathogenesis, Diagnosis, Treatment, and Prevention.Viruses · 2023Review
- Hantavirus: an overview and advancements in therapeutic approaches for infection.Frontiers in microbiology · 2023Review
- The kidney in hantavirus infection-epidemiology, virology, pathophysiology, clinical presentation, diagnosis and management.Clinical kidney journal · 2022Review
- Hemorrhagic Fever with Renal Syndrome: Literature Review, Epidemiology, Clinical Picture and Pathogenesis.Infection & chemotherapy · 2022Review
- Immune response during hantavirus diseases: implications for immunotherapies and vaccine design.Immunology · 2021Review
- HTNV infection of CD8Communications biology · 2021Article
- Viruses Run: The Evasion Mechanisms of the Antiviral Innate Immunity by Hantavirus.Frontiers in microbiology · 2021Review
- The Presence of Circulating Nucleated Red Blood Cells Is Associated With Disease Severity in Patients of Hemorrhagic Fever With Renal Syndrome.Frontiers in medicine · 2021Article
- Devilishly radical NETwork in COVID-19: Oxidative stress, neutrophil extracellular traps (NETs), and T cell suppression.Advances in biological regulation · 2020Review
- Replication in the Mononuclear Phagocyte System (MPS) as a Determinant of Hantavirus Pathogenicity.Frontiers in cellular and infection microbiology · 2020Article
- Review
- Motility of human renal cells is disturbed by infection with pathogenic hantaviruses.BMC infectious diseases · 2018Article
- Kyasanur Forest disease virus infection activates human vascular endothelial cells and monocyte-derived dendritic cells.Emerging microbes & infections · 2018Article
- The nucleocapsid protein of hantaviruses: much more than a genome-wrapping protein.Virus genes · 2018Review
- Hantavirus-Driven PD-L1/PD-L2 Upregulation: An Imperfect Viral Immune Evasion Mechanism.Frontiers in immunology · 2018Article
- Human hantavirus infection elicits pronounced redistribution of mononuclear phagocytes in peripheral blood and airways.PLoS pathogens · 2017Article
- Exploring the Immunopathogenesis of Viral Hemorrhagic Fever in Mice with a Humanized Immune System.Frontiers in immunology · 2017Review
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dendritic cells (DCs) play a pivotal role as antigen-presenting cells in the antiviral immune response. Here we show that Hantaan virus (HTNV), which belongs to the Bunyaviridae family (genus Hantavirus) and causes hemorrhagic fever with renal syndrome, productively infects human DCs in vitro. In the course of HTNV infection, DCs did not show any cytopathic effect and viral replication did not induce cell lysis or apoptosis. Furthermore, HTNV did not affect apoptosis-inducing signals that are important for the homeostatic control of mature DCs. In contrast to immunosuppressive viruses, e.g., human cytomegalovirus, HTNV activated immature DCs, resulting in upregulation of major histocompatibility complex (MHC), costimulatory, and adhesion molecules. Intriguingly, strong upregulation of MHC class I molecules and an increased intercellular cell adhesion molecule type 1 expression was also detected on HTNV-infected endothelial cells. In addition, antigen uptake by HTNV-infected DCs was reduced, another characteristic feature of DC maturation. Consistent with these findings, we observed that HTNV-infected DCs stimulated T cells as efficiently as did mature DCs. Finally, infection of DCs with HTNV induced the release of the proinflammatory cytokines tumor necrosis factor alpha and alpha interferon. Taken together, our findings indicate that hantavirus-infected DCs may significantly contribute to hantavirus-associated pathogenesis.
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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.