Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (792 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
A form of meningitis caused by lymphocytic choriomeningitis virus. MICE and other rodents serve as the natural hosts, and infection in humans usually occurs through inhalation or ingestion of infectious particles. Clinical manifestations include an influenza-like syndrome followed by stiff neck, alterations of mentation, ataxia, and incontinence. Maternal infections may result in fetal malformations and injury, including neonatal hydrocephalus, aqueductal stenosis, chorioretinitis, and microcephaly. (From Joynt, Clinical Neurology, 1996, Ch26, pp1-3)
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Choriomeningitis, Lymphocytic; Armstrong Syndrome; Syndrome, Armstrong; Armstrong's Syndrome; Syndrome, Armstrong's; Encephalomyelitis, Lymphocytic Choriomeningitis Virus; Lymphocytic Choriomeningitis Virus Encephalomyelitis.
Where it fits in the MeSH classification
- Broader topics
- Meningitis, Viral; Arenaviridae Infections
Related concepts
- Lymphocytic Choriomeningitis Virus
- Ataxia
- Hydrocephalus
- Chorioretinitis
- Microcephaly
Research landscape
PubMed indexes 2,474 records tagged with the MeSH heading “Lymphocytic Choriomeningitis” (counts retrieved 2026-10-29). 296 of them (12.0%) were published from 2020 onward, and the busiest period so far is through 1999 with 1,256 records.
Reviews account for 164 records (6.6%) and meta-analyses for 0. Randomized controlled trials number 0 (0.0%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 1,256 |
| 2000-2009 | 416 |
| 2010-2019 | 506 |
| 2020 onward | 296 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 164 | 6.6% |
| Meta-analyses | 0 | 0.0% |
| Randomized controlled trials | 0 | 0.0% |
Method: PubMed query "Lymphocytic Choriomeningitis"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.
Reading the evidence in infectious diseases
Infectious disease evidence combines microbiology, epidemiology and clinical trials. Laboratory studies identify pathogens and how they cause harm; surveillance and outbreak investigations describe who is affected and how infection spreads; trials establish whether treatments and vaccines work. Results depend on place and time, because pathogens evolve and resistance patterns and population immunity change. Check when and where the data were collected, how cases were defined and how up to date the evidence is.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| A role for the chemokine RANTES in regulating CD8 T cell responses during chronic viral infection | 2011 | Research article Design not recorded in structured metadata | 161 | cc by PMID 21814510 · DOI · PMC3141034 |
| Type I interferon signaling attenuates regulatory T cell function in viral infection and in the tumor microenvironment | 2018 | Research article Design not recorded in structured metadata | 108 | cc0 PMID 29672594 · DOI · PMC5929570 |
| Rapid in vitro generation of bona fide exhausted CD8+ T cells is accompanied by Tcf7 promotor methylation | 2020 | Research article Design not recorded in structured metadata | 72 | cc by PMID 32579593 · DOI · PMC7340326 |
| Stromal Cell-Mast Cell Communication Orchestrates Anti-Viral Immunity in the Meninges | 2026 | Research article Design not recorded in structured metadata | 4 | cc by PMID 41195564 · DOI · PMC12850450 |
A role for the chemokine RANTES in regulating CD8 T cell responses during chronic viral infection [1]
Abstract reading summary — source excerpts
- Opening excerpt
- RANTES (CCL5) is a chemokine expressed by many hematopoietic and non-hematopoietic cell types that plays an important role in homing and migration of effector and memory T cells during acute infections.
- Closing excerpt
- Our results demonstrate an important role for RANTES in sustaining CD8 T cell responses during a systemic chronic viral infection.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (215 words)
RANTES (CCL5) is a chemokine expressed by many hematopoietic and non-hematopoietic cell types that plays an important role in homing and migration of effector and memory T cells during acute infections. The RANTES receptor, CCR5, is a major target of anti-HIV drugs based on blocking viral entry. However, defects in RANTES or RANTES receptors including CCR5 can compromise immunity to acute infections in animal models and lead to more severe disease in humans infected with west Nile virus (WNV). In contrast, the role of the RANTES pathway in regulating T cell responses and immunity during chronic infection remains unclear. In this study, we demonstrate a crucial role for RANTES in the control of systemic chronic LCMV infection. In RANTES⁻/⁻ mice, virus-specific CD8 T cells had poor cytokine production. These RANTES⁻/⁻ CD8 T cells also expressed higher amounts of inhibitory receptors consistent with more severe exhaustion. Moreover, the cytotoxic ability of CD8 T cells from RANTES⁻/⁻ mice was reduced. Consequently, viral load was higher in the absence of RANTES. The dysfunction of T cells in the absence of RANTES was as severe as CD8 T cell responses generated in the absence of CD4 T cell help. Our results demonstrate an important role for RANTES in sustaining CD8 T cell responses during a systemic chronic viral infection.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 21814510 · DOI · PMC3141034
Type I interferon signaling attenuates regulatory T cell function in viral infection and in the tumor microenvironment [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Regulatory T cells (Tregs) play a cardinal role in the immune system by suppressing detrimental autoimmune responses, but their role in acute, chronic infectious diseases and tumor microenvironment remains unclear.
- Closing excerpt
- Thus, IFN signaling in Tregs is beneficial to host resulting in a more effective antiviral response and augmented antitumor immunity.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (226 words)
Regulatory T cells (Tregs) play a cardinal role in the immune system by suppressing detrimental autoimmune responses, but their role in acute, chronic infectious diseases and tumor microenvironment remains unclear. We recently demonstrated that IFN-α/β receptor (IFNAR) signaling promotes Treg function in autoimmunity. Here we dissected the functional role of IFNAR-signaling in Tregs using Treg-specific IFNAR deficient (IFNARfl/flxFoxp3YFP-Cre) mice in acute LCMV Armstrong, chronic Clone-13 viral infection, and in tumor models. In both viral infection and tumor models, IFNARfl/flxFoxp3YFP-Cre mice Tregs expressed enhanced Treg associated activation antigens. LCMV-specific CD8+ T cells and tumor infiltrating lymphocytes from IFNARfl/flxFoxp3YFP-Cre mice produced less antiviral and antitumor IFN-γ and TNF-α. In chronic viral model, the numbers of antiviral effector and memory CD8+ T cells were decreased in IFNARfl/flxFoxp3YFP-Cre mice and the effector CD4+ and CD8+ T cells exhibited a phenotype compatible with enhanced exhaustion. IFNARfl/flxFoxp3YFP-Cre mice cleared Armstrong infection normally, but had higher viral titers in sera, kidneys and lungs during chronic infection, and higher tumor burden than the WT controls. The enhanced activated phenotype was evident through transcriptome analysis of IFNARfl/flxFoxp3YFP-Cre mice Tregs during infection demonstrated differential expression of a unique gene signature characterized by elevated levels of genes involved in suppression and decreased levels of genes mediating apoptosis. Thus, IFN signaling in Tregs is beneficial to host resulting in a more effective antiviral response and augmented antitumor immunity.
Abstract reproduced from the open-access article under the recorded cc0 licence; © the authors. PMID 29672594 · DOI · PMC5929570
Rapid in vitro generation of bona fide exhausted CD8+ T cells is accompanied by Tcf7 promotor methylation [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Exhaustion is a dysfunctional state of cytotoxic CD8+ T cells (CTL) observed in chronic infection and cancer.
- Closing excerpt
- Thus this novel in vitro system can be used to identify genes and signaling pathways involved in exhaustion and will facilitate the screening of reagents that prevent/reverse CTL exhaustion.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (207 words)
Exhaustion is a dysfunctional state of cytotoxic CD8+ T cells (CTL) observed in chronic infection and cancer. Current in vivo models of CTL exhaustion using chronic viral infections or cancer yield very few exhausted CTL, limiting the analysis that can be done on these cells. Establishing an in vitro system that rapidly induces CTL exhaustion would therefore greatly facilitate the study of this phenotype, identify the truly exhaustion-associated changes and allow the testing of novel approaches to reverse or prevent exhaustion. Here we show that repeat stimulation of purified TCR transgenic OT-I CTL with their specific peptide induces all the functional (reduced cytokine production and polyfunctionality, decreased in vivo expansion capacity) and phenotypic (increased inhibitory receptors expression and transcription factor changes) characteristics of exhaustion. Importantly, in vitro exhausted cells shared the transcriptomic characteristics of the gold standard of exhaustion, CTL from LCMV cl13 infections. Gene expression of both in vitro and in vivo exhausted CTL was distinct from T cell anergy. Using this system, we show that Tcf7 promoter DNA methylation contributes to TCF1 downregulation in exhausted CTL. Thus this novel in vitro system can be used to identify genes and signaling pathways involved in exhaustion and will facilitate the screening of reagents that prevent/reverse CTL exhaustion.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 32579593 · DOI · PMC7340326
Stromal Cell-Mast Cell Communication Orchestrates Anti-Viral Immunity in the Meninges [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Mast cells are tissue-resident immune sentinels.
- Closing excerpt
- Collectively, these findings reveal a critical role for mast cells in enhancing meningeal antiviral immunity and highlight potential strategies for brain protection during infection.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (144 words)
Mast cells are tissue-resident immune sentinels. However, their spatial localization and potential role in the antiviral response within the meninges-the protective barrier surrounding the central nervous system-remain unclear. Here, the distribution pattern along meningeal vasculature is maped and identified a post-weaning maturation process. Single-cell RNA sequencing reveals that mast cells mount a robust immune response against LCMV infection. Ablation of mast cells results in reduced CD8+ T cell infiltration and impairs viral clearance. Mechanistic dissection identifies a critical role for the IL-33 receptor on mast cells, which responds to IL-33 derived from stromal cells, in mediating antiviral immunity. Further analysis shows that mast cells synergistically upregulate cytokines and chemokines in response to IL-33 and ATP released by virus-infected stromal cells. Collectively, these findings reveal a critical role for mast cells in enhancing meningeal antiviral immunity and highlight potential strategies for brain protection during infection.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41195564 · DOI · PMC12850450
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article The virology and immunobiology of lymphocytic choriomeningitis virus infection [5]
- Research article CD8 T cell dysfunction during chronic viral infection [6]
- Research article T-cell-mediated immunopathology in viral infections [7]
- Research article Lymphocytic choriomeningitis virus: an underrecognized cause of neurologic disease in the fetus, child, and adult [8]
- Research article Biology and pathogenesis of lymphocytic choriomeningitis virus infection [9]
- Research article Congenital lymphocytic choriomeningitis virus infection: decade of rediscovery [10]
References
- Crawford A, Angelosanto JM, Nadwodny KL, Blackburn SD, Wherry EJ. A role for the chemokine RANTES in regulating CD8 T cell responses during chronic viral infection. . 2011. PMID 21814510 · DOI · PMC3141034
- Gangaplara A, Martens C, Dahlstrom E, Metidji A, Gokhale AS, Glass DD, et al.. Type I interferon signaling attenuates regulatory T cell function in viral infection and in the tumor microenvironment. . 2018. PMID 29672594 · DOI · PMC5929570
- Zhao M, Kiernan CH, Stairiker CJ, Hope JL, Leon LG, van Meurs M, et al.. Rapid in vitro generation of bona fide exhausted CD8+ T cells is accompanied by Tcf7 promotor methylation. . 2020. PMID 32579593 · DOI · PMC7340326
- Li Q, Chen W, Sun M, Ni X, Ran Q, Hu X, et al.. Stromal Cell-Mast Cell Communication Orchestrates Anti-Viral Immunity in the Meninges. . 2026. PMID 41195564 · DOI · PMC12850450
- Buchmeier MJ, Welsh RM, Dutko FJ, Oldstone MB. The virology and immunobiology of lymphocytic choriomeningitis virus infection. Adv Immunol. 1980. PMID 6160740 · DOI
- Shin H, Wherry EJ. CD8 T cell dysfunction during chronic viral infection. Curr Opin Immunol. 2007. PMID 17656078 · DOI
- Doherty PC, Zinkernagel RM. T-cell-mediated immunopathology in viral infections. Transplant Rev. 1974. PMID 4601807 · DOI
- Bonthius DJ. Lymphocytic choriomeningitis virus: an underrecognized cause of neurologic disease in the fetus, child, and adult. Semin Pediatr Neurol. 2012. PMID 22889536 · DOI · PMC4256959
- Oldstone MB. Biology and pathogenesis of lymphocytic choriomeningitis virus infection. Curr Top Microbiol Immunol. 2002. PMID 11987822 · DOI
- Barton LL, Mets MB. Congenital lymphocytic choriomeningitis virus infection: decade of rediscovery. Clin Infect Dis. 2001. PMID 11438904 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-29.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.