ArticleJournal of virology2006
Altered central nervous system gene expression caused by congenitally acquired persistent infection with lymphocytic choriomeningitis virus.
Article in Journal of virology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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.
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.
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Who cites it
23 citing papers in PubMed, 33 citations in OpenAlex.
- Nociceptor neurons shape antiviral immunity.Journal of neuroinflammation · 2026Review
- Chronic infection perturbs the affinity hierarchy of antiviral B cells.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Ecology of Lassa Virus.Current topics in microbiology and immunology · 2023Article
- Animal Models of Enterovirus D68 Infection and Disease.Journal of virology · 2022Review
- Neuroinvasion and cognitive impairment in comorbid alcohol dependence and chronic viral infection: An initial investigation.Journal of neuroimmunology · 2019Article
- Arenavirus infection correlates with lower survival of its natural rodent host in a long-term capture-mark-recapture study.Parasites & vectors · 2018Article
- Alcohol intake alters immune responses and promotes CNS viral persistence in mice.Behavioural brain research · 2016Article
- Therapeutic antiviral T cells noncytopathically clear persistently infected microglia after conversion into antigen-presenting cells.The Journal of experimental medicine · 2015Article
- CCR5 knockout prevents neuronal injury and behavioral impairment induced in a transgenic mouse model by a CXCR4-using HIV-1 glycoprotein 120.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- Article
- Distinct neural stem cell tropism, early immune activation, and choroid plexus pathology following coxsackievirus infection in the neonatal central nervous system.Laboratory investigation; a journal of technical methods and pathology · 2014Article
- Article
- Type I interferon programs innate myeloid dynamics and gene expression in the virally infected nervous system.PLoS pathogens · 2013Article
- Neuro-invasion by a 'Trojan Horse' strategy and vasculopathy during intrauterine flavivirus infection.International journal of experimental pathology · 2012Article
- Article
- Targeting the proteolytic processing of the viral glycoprotein precursor is a promising novel antiviral strategy against arenaviruses.Journal of virology · 2010Article
- Identification of amino acid residues critical for the anti-interferon activity of the nucleoprotein of the prototypic arenavirus lymphocytic choriomeningitis virus.Journal of virology · 2009Article
- Persistent viral infection elevates central nervous system MHC class I through chronic production of interferons.Journal of immunology (Baltimore, Md. : 1950) · 2009Article
- Response and recovery in the plasma metabolome tracks the acute LCMV-induced immune response.Journal of proteome research · 2009Article
- Lymphocytic choriomeningitis infection of the central nervous system.Frontiers in bioscience : a journal and virtual library · 2008Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Neonatal infection of most mouse strains with lymphocytic choriomeningitis virus (LCMV) leads to a life-long persistent infection characterized by high virus loads in the central nervous system (CNS) in the absence of inflammation and tissue destruction. These mice, however, exhibit impaired learning and memory. The occurrence of cognitive defects in the absence of overt CNS pathology led us to the hypothesis that chronic virus infection may contribute to neuronal dysfunction by altering the host's gene expression profile. To test this hypothesis, we examined the impact of LCMV persistence on host gene expression in the CNS. To model the natural route of human congenital CNS infection observed with a variety of viruses, we established a persistently infected mouse colony where the virus was maintained via vertical transmission from infected mothers to offspring (LCMV-cgPi). LCMV-cgPi mice exhibited a lifelong persistent infection involving the CNS; the infection was associated with impaired spatial-temporal learning. Despite high viral loads in neurons of the brains of adult LCMV-cgPi mice, we detected changes in the host's CNS gene expression for only 75 genes, 56 and 19 being significantly induced and reduced, respectively. The majority of the genes induced in the brain of LCMV-cgPi mice were interferon (IFN)-stimulated genes (ISGs) and included the transcription factors STAT1 and IRF9, the ISG15 protease UBP43, and the glucocorticoid attenuated-response genes GARG16 and GARG49. Based on their crucial role in antiviral defense, these ISGs may play an important role in limiting viral spread and replication. However, since IFNs have also been implicated in adverse effects on neuronal function, the chronic induction of some ISGs may also contribute to the observed cognitive impairment.
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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.