ArticleImmunology2013
The adaptive immune response does not influence hantavirus disease or persistence in the Syrian hamster.
Article in Immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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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
31 citing papers in PubMed, 45 citations in OpenAlex.
- High genomic stability of Andes virus following successive passageJournal of virology · 2025Article
- Human-to-Human Transmission of Andes Virus Modeled in Syrian Hamsters.Emerging infectious diseases · 2023Article
- Dual spike and nucleocapsid mRNA vaccination confer protection against SARS-CoV-2 Omicron and Delta variants in preclinical models.Science translational medicine · 2022Article
- Innate Immunity to Orthohantaviruses: Could Divergent Immune Interactions Explain Host-specific Disease Outcomes?Journal of molecular biology · 2022Review
- Progression and Resolution of Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) Infection in Golden Syrian Hamsters.The American journal of pathology · 2022Article
- An immune-competent, replication-permissive Syrian Hamster glioma model for evaluating Delta-24-RGD oncolytic adenovirus.Neuro-oncology · 2021Article
- Binding of the Andes Virus Nucleocapsid Protein to RhoGDI Induces the Release and Activation of the Permeability Factor RhoA.Journal of virology · 2021Article
- Pathogenic and transcriptomic differences of emerging SARS-CoV-2 variants in the Syrian golden hamster model.bioRxiv : the preprint server for biology · 2021Article
- Differential pathogenesis between Andes virus strains CHI-7913 and Chile-9717869in Syrian Hamsters.Journal of virology · 2021Article
- Natural killer cell responses to emerging viruses of zoonotic origin.Current opinion in virology · 2020Review
- Hantavirus infection in type I interferon receptor-deficient (A129) mice.The Journal of general virology · 2020Article
- Unique Interferon Pathway Regulation by the Andes Virus Nucleocapsid Protein Is Conferred by Phosphorylation of Serine 386.Journal of virology · 2019Article
- Syrian Hamster as an Animal Model for the Study on Infectious Diseases.Frontiers in immunology · 2019Review
- Two recombinant human monoclonal antibodies that protect against lethal Andes hantavirus infection in vivo.Science translational medicine · 2018Article
- Involvement of Pro-Inflammatory Macrophages in Liver Pathology of Pirital Virus-Infected Syrian Hamsters.Viruses · 2018Article
- A lethal disease model for New World hantaviruses using immunosuppressed Syrian hamsters.PLoS neglected tropical diseases · 2017Article
- Serum Cytokine Profiles Differentiating Hemorrhagic Fever with Renal Syndrome and Hantavirus Pulmonary Syndrome.Frontiers in immunology · 2017Article
- Syrian Hamsters as a Small Animal Model for Emerging Infectious Diseases: Advances in Immunologic Methods.Advances in experimental medicine and biology · 2017Article
- Article
- Depletion of Alveolar Macrophages Does Not Prevent Hantavirus Disease Pathogenesis in Golden Syrian Hamsters.Journal of virology · 2016Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Pathogenic New World hantaviruses cause severe disease in humans characterized by a vascular leak syndrome, leading to pulmonary oedema and respiratory distress with case fatality rates approaching 40%. Hantaviruses infect microvascular endothelial cells without conspicuous cytopathic effects, indicating that destruction of the endothelium is not a mechanism of disease. In humans, high levels of inflammatory cytokines are present in the lungs of patients that succumb to infection. This, along with other observations, suggests that disease has an immunopathogenic component. Currently the only animal model available to study hantavirus disease is the Syrian hamster, where infection with Andes virus (ANDV), the primary agent of disease in South America, results in disease that closely mimics that seen in humans. Conversely, inoculation of hamsters with a passaged Sin Nombre virus (SNV), the virus responsible for most cases of disease in North America, results in persistent infection with high levels of viral replication. We found that ANDV elicited a stronger innate immune response, whereas SNV elicited a more robust adaptive response in the lung. Additionally, ANDV infection resulted in significant changes in the blood lymphocyte populations. To determine whether the adaptive immune response influences infection outcome, we depleted hamsters of CD4(+) and CD8(+) T cells before infection with hantaviruses. Depletion resulted in inhibition of virus-specific antibody responses, although the pathogenesis and replication of these viruses were unaltered. These data show that neither hantavirus replication, nor pathogenesis caused by these viruses, is influenced by the adaptive immune response in the Syrian hamster.
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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.