ArticleProceedings of the National Academy of Sciences of the United States of America2018
Lymphocytic choriomeningitis virus Clone 13 infection causes either persistence or acute death dependent on IFN-1, cytotoxic T lymphocytes (CTLs), and host genetics.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 48 citations in OpenAlex.
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- Development and protective evaluation of mRNA vaccines encoding the glycoprotein precursor of lymphocytic choriomeningitis virus.Virus research · 2026Article
- Krüppel-like factors 2 and 3 regulate T cell exhaustion by directing T cell residency and migration.Immunity · 2026Article
- Site-1 protease mediated GPC processing is required for persistence of LCMV Clone 13.Npj viruses · 2026Article
- Early sex-related transcriptional differences in CD8Frontiers in immunology · 2026Article
- Checkpoint-enriched T cells with retained effector-associated features are associated with disease activity in systemic lupus erythematosus.Frontiers in immunology · 2026Article
- Lpar5 regulates the CD8 T-cell response to persistent virus infection by altering exhaustion programming, survival, and NK receptor expression.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- Optimized arenaviruses with tumor-tropic mutations promote safe anti-tumor efficacy via sustainable immune modulatory properties.Cell reports. Medicine · 2025Article
- Unraveling the complexities of neurotropic virus infection and immune evasion.Microbiology and molecular biology reviews : MMBR · 2025Review
- Pathogenicity of tick-derived lymphocytic choriomeningitis virus in BALB/c mice.BMC veterinary research · 2025Article
- ISG15 Drives Immune Pathology and Respiratory Failure during Systemic Lymphocytic Choriomeningitis Virus Infection.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- Characterization of Collaborative Cross mouse founder strain CAST/EiJ as a novel model for lethal COVID-19.Scientific reports · 2024Article
- Characterization of Collaborative Cross mouse founder strain CAST/EiJ as a novel model for lethal COVID-19.Research square · 2024Article
- An mRNA-LNP-based Lassa virus vaccine induces protective immunity in mice.Journal of virology · 2024Article
- Type I interferons induce an epigenetically distinct memory B cell subset in chronic viral infection.Immunity · 2024Article
- Autoimmunity-associated allele of tyrosine phosphatase gene PTPN22 enhances anti-viral immunity.PLoS pathogens · 2024Article
- Complementary HLH susceptibility factors converge on CD8 T-cell hyperactivation.Blood advances · 2023Article
- Mice with FVB-derived sequence on chromosome 17 succumb to disseminated virus infection due to aberrant NK cell and T cell responses.iScience · 2023Article
- Lymphocytic Choriomeningitis Virus Clone 13 Infection Results in CD8 T Cell-Mediated Host Mortality in Diacylglycerol Kinase α-Deficient Mice.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Genetic Mapping of Behavioral Traits Using the Collaborative Cross Resource.International journal of molecular sciences · 2022Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Understanding of T cell exhaustion and successful therapy to restore T cell function was first described using Clone (Cl) 13 variant selected from the lymphocytic choriomeningitis virus (LCMV) Armstrong (ARM) 53b parental strain. T cell exhaustion plays a pivotal role in both persistent infections and cancers of mice and humans. C57BL/6, BALB, SWR/J, A/J, 129, C3H, and all but one collaborative cross (CC) mouse strain following Cl 13 infection have immunosuppressed T cell responses, high PD-1, and viral titers leading to persistent infection and normal life spans. In contrast, the profile of FVB/N, NZB, PL/J, SL/J, and CC NZO mice challenged with Cl 13 is a robust T cell response, high titers of virus, PD-1, and Lag3 markers on T cells. These mice all die 7 to 9 d after Cl 13 infection. Death is due to enhanced pulmonary endothelial vascular permeability, pulmonary edema, collapse of alveolar air spaces, and respiratory failure. Pathogenesis involves abundant levels of Cl 13 receptor alpha-dystroglycan on endothelial cells, with high viral replication in such cells leading to immunopathologic injury. Death is aborted by blockade of interferon-1 (IFN-1) signaling or deletion of CD8 T cells.
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