ArticleThe Journal of general virology2016
Interferon gamma modulation of disease manifestation and the local antibody response to alphavirus encephalomyelitis.
Article in The Journal of general virology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
21 citing papers in PubMed, 30 citations in OpenAlex.
- The pathogenicity and virulence of Sindbis virus.Virulence · 2026Review
- Characterization of an immunocompetent, young adult mouse model for studying chikungunya virus neuroinvasion and central nervous system infection.PLoS pathogens · 2026Article
- Infectious and Immunological Links Between Periodontitis and COVID-19: A Review.Medical science monitor : international medical journal of experimental and clinical research · 2025Review
- Neuropathogenesis of Old World Alphaviruses: Considerations for the Development of Medical Countermeasures.Viruses · 2025Review
- Article
- EGR1 Upregulation during Encephalitic Viral Infections Contributes to Inflammation and Cell Death.Viruses · 2022Article
- Between immunomodulation and immunotolerance: The role of IFNγ in SARS-CoV-2 disease.Cytokine · 2021Review
- Production of Noncapped Genomic RNAs Is Critical to Sindbis Virus Disease and Pathogenicity.mBio · 2020Article
- Evaluation in Swine of a Recombinant African Swine Fever Virus Lacking the MGF-360-1L Gene.Viruses · 2020Article
- Disruption of Zika Virus xrRNA1-Dependent sfRNA1 Production Results in Tissue-Specific Attenuated Viral Replication.Viruses · 2020Article
- Astrocyte Reactivity: Subtypes, States, and Functions in CNS Innate Immunity.Trends in immunology · 2020Review
- Type II interferon signaling in the brain during a viral infection with age-dependent pathogenesis.Developmental neurobiology · 2020Article
- Interferon-Gamma Modulation of the Local T Cell Response to Alphavirus Encephalomyelitis.Viruses · 2020Article
- Immunopathogenesis of alphaviruses.Advances in virus research · 2020Article
- CpG Oligonucleotides Protect Mice From Alphavirus Encephalitis: Role of NK Cells, Interferons, and TNF.Frontiers in immunology · 2020Article
- Protease-activated receptor 4 protects mice from Coxsackievirus B3 and H1N1 influenza A virus infection.Cellular immunology · 2019Article
- Neuroinflammation During RNA Viral Infections.Annual review of immunology · 2019Review
- Genetic control of alphavirus pathogenesis.Mammalian genome : official journal of the International Mammalian Genome Society · 2018Review
- Germ Line IgM Is Sufficient, but Not Required, for Antibody-Mediated Alphavirus Clearance from the Central Nervous System.Journal of virology · 2018Article
- Death and gastrointestinal bleeding complicate encephalomyelitis in mice with delayed appearance of CNS IgM after intranasal alphavirus infection.The Journal of general virology · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Infection of mice with Sindbis virus (SINV) produces encephalomyelitis and provides a model for examination of the central nervous system (CNS) immune response to alphavirus infection. Clearance of infectious virus is accomplished through a cooperative effort between SINV-specific antibody and IFN-γ, but the regulatory interactions are poorly understood. To determine the effects of IFN-γ on clinical disease and the antiviral immune response, C57BL/6 mice lacking IFN-γ (Ifng-/-) or IFN-γ receptor (Ifngr1-/-) were studied in comparison to WT mice. Maximum production of Ifng mRNA and IFN-γ protein in the CNS of WT and Ifngr1-/- mice occurred 5-7 days after infection, with higher levels of IFN-γ in Ifngr1-/- mice. Onset of clinical disease was earlier in mice with impaired IFN-γ signalling, although Ifngr1-/- mice recovered more rapidly. Ifng-/- and Ifngr1-/- mice maintained body weight better than WT mice, associated with better food intake and lower brain levels of inflammatory cytokines. Clearance of infectious virus from the spinal cords was slower, and CNS, but not serum, levels of SINV-specific IgM, IgG2a and IgG2b were lower in Ifngr1-/- and Ifng-/- mice compared to WT mice. Decreased CNS antiviral antibody was associated with lower expression of mRNAs for B-cell attracting chemokines CXCL9, CXCL10 and CXCL13 and fewer B cells in the CNS. Therefore, IFN-γ signalling increases levels of CNS pro-inflammatory cytokines, leading to clinical disease, but synergistically clears virus with SINV-specific antibody at least in part by increasing chemokine production important for infiltration of antibody-secreting B cells into the CNS.
Indexed as
Identifiers
What OpenQuestion holds
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.