ArticlePLoS pathogens2016
Type I Interferons Direct Gammaherpesvirus Host Colonization.
Article in PLoS pathogens, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 15 citations in OpenAlex.
- Genetic background modifies host and viral parameters of neonatal gammaherpesvirus infection.Journal of virology · 2026Article
- Conserved gammaherpesvirus protein kinase counters myeloid cell-specific type I IFN receptor but not IRF-3 expression to promote the establishment of chronic latent infection in the spleen.Journal of virology · 2026Article
- IL-22 promotes the establishment of chronic gammaherpesvirus infection by supporting the germinal center response.PLoS pathogens · 2026Article
- Gammaherpesvirus infection unveils exaggerated germinal center responses in an SR-BI-deficient host.Journal of virology · 2025Article
- Apolipoprotein E selectively supports gammaherpesvirus replication in macrophages.Journal of virology · 2025Article
- STAT1 and herpesviruses: Making lemonade from lemons.Virology · 2025Review
- Review
- Article
- Conserved Gammaherpesvirus Protein Kinase Counters the Antiviral Effects of Myeloid Cell-Specific STAT1 Expression To Promote the Establishment of Splenic B Cell Latency.Journal of virology · 2021Article
- Interferon Regulatory Factor 3 Supports the Establishment of Chronic Gammaherpesvirus Infection in a Route- and Dose-Dependent Manner.Journal of virology · 2021Article
- Th2 Cytokine Modulates Herpesvirus Reactivation in a Cell Type Specific Manner.Journal of virology · 2021Article
- Review
- Interferon Regulatory Factor 7 Attenuates Chronic Gammaherpesvirus Infection.Journal of virology · 2020Article
- In Vivo Imaging-Driven Approaches to Study Virus Dissemination and Pathogenesis.Annual review of virology · 2019Review
- Article
- Type I Interferon Signaling to Dendritic Cells Limits Murid Herpesvirus 4 Spread from the Olfactory Epithelium.Journal of virology · 2017Article
- The replication and transcription activator of murine gammaherpesvirus 68 cooperatively enhances cytokine-activated, STAT3-mediated gene expression.The Journal of biological chemistry · 2017Article
- Type I Interferons and NK Cells Restrict Gammaherpesvirus Lymph Node Infection.Journal of virology · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gamma-herpesviruses colonise lymphocytes. Murid Herpesvirus-4 (MuHV-4) infects B cells via epithelial to myeloid to lymphoid transfer. This indirect route entails exposure to host defences, and type I interferons (IFN-I) limit infection while viral evasion promotes it. To understand how IFN-I and its evasion both control infection outcomes, we used Mx1-cre mice to tag floxed viral genomes in IFN-I responding cells. Epithelial-derived MuHV-4 showed low IFN-I exposure, and neither disrupting viral evasion nor blocking IFN-I signalling markedly affected acute viral replication in the lungs. Maximising IFN-I induction with poly(I:C) increased virus tagging in lung macrophages, but the tagged virus spread poorly. Lymphoid-derived MuHV-4 showed contrastingly high IFN-I exposure. This occurred mainly in B cells. IFN-I induction increased tagging without reducing viral loads; disrupting viral evasion caused marked attenuation; and blocking IFN-I signalling opened up new lytic spread between macrophages. Thus, the impact of IFN-I on viral replication was strongly cell type-dependent: epithelial infection induced little response; IFN-I largely suppressed macrophage infection; and viral evasion allowed passage through B cells despite IFN-I responses. As a result, IFN-I and its evasion promoted a switch in infection from acutely lytic in myeloid cells to chronically latent in B cells. Murine cytomegalovirus also showed a capacity to pass through IFN-I-responding cells, arguing that this is a core feature of herpesvirus host colonization.
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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.