ArticleViruses2015
Elevated cytokines, thrombin and PAI-1 in severe HCPS patients due to Sin Nombre virus.
Article in Viruses, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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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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
16 citing papers in PubMed, 29 citations in OpenAlex.
- Omics Approaches in Hantavirus Research: Current Advances, Challenges, and Future Perspectives.Biotech (Basel (Switzerland)) · 2026Review
- Hantavirus Emergence in a Changing World: Virology, Pathogenesis, Surveillance, and One Health Preparedness.Microorganisms · 2026Review
- Potential Mechanisms Underlying Bleeding During Infection With Hemorrhagic Fever Viruses.Arteriosclerosis, thrombosis, and vascular biology · 2026Review
- Pathogenicity and virulence of Rodent-Borne Orthohantaviruses.Virulence · 2025Review
- Seoul orthohantavirus evades innate immune activation by reservoir endothelial cells.PLoS pathogens · 2024Article
- Levels of peripheral blood routine, biochemical and coagulation parameters in patients with hemorrhagic fever with renal syndrome and their relationship with prognosis: an observational cohort study.BMC infectious diseases · 2024Observational
- Article
- Exploration of the effects of goose TCs on GCs at different follicular stages using a co-culture model.Bioscience reports · 2020Article
- RIG-I-like receptor activation drives type I IFN and antiviral signaling to limit Hantaan orthohantavirus replication.PLoS pathogens · 2020Article
- Differential Regulation of PAI-1 in Hantavirus Cardiopulmonary Syndrome and Hemorrhagic Fever With Renal Syndrome.Open forum infectious diseases · 2018Article
- Small-Volume Flow Cytometry-Based Multiplex Analysis of the Activity of Small GTPases.Methods in molecular biology (Clifton, N.J.) · 2018Article
- Upregulation of P2YFrontiers in cellular and infection microbiology · 2018Article
- Protease-activated receptor 1 inhibition protects mice against thrombin-dependent respiratory syncytial virus and human metapneumovirus infections.British journal of pharmacology · 2018Article
- Serum levels of interleukin-6 are linked to the severity of the disease caused by Andes Virus.PLoS neglected tropical diseases · 2017Article
- Hantavirus Infection Suppresses Thrombospondin-1 Expression in Cultured Endothelial Cells in a Strain-Specific Manner.Frontiers in microbiology · 2016Article
- Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Sin Nombre Hantavirus (SNV, Bunyaviridae Hantavirus) is a Category A pathogen that causes Hantavirus Cardiopulmonary Syndrome (HCPS) with case fatality ratios generally ranging from 30% to 50%. HCPS is characterized by vascular leakage due to dysregulation of the endothelial barrier function. The loss of vascular integrity results in non-cardiogenic pulmonary edema, shock, multi-organ failure and death. Using Electric Cell-substrate Impedance Sensing (ECIS) measurements, we found that plasma samples drawn from University of New Mexico Hospital patients with serologically-confirmed HCPS, induce loss of cell-cell adhesion in confluent epithelial and endothelial cell monolayers grown in ECIS cultureware. We show that the loss of cell-cell adhesion is sensitive to both thrombin and plasmin inhibitors in mild cases, and to thrombin only inhibition in severe cases, suggesting an increasing prothrombotic state with disease severity. A proteomic profile (2D gel electrophoresis and mass spectrometry) of HCPS plasma samples in our cohort revealed robust antifibrinolytic activity among terminal case patients. The prothrombotic activity is highlighted by acute ≥30 to >100 fold increases in active plasminogen activator inhibitor (PAI-1) which, preceded death of the subjects within 48 h. Taken together, this suggests that PAI-1 might be a response to the severe pathology as it is expected to reduce plasmin activity and possibly thrombin activity in the terminal patients.
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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.