ArticleJournal of virology2022
Interferon Alpha, but Not Interferon Beta, Acts Early To Control Chronic Chikungunya Virus Pathogenesis.
Article in Journal of virology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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
28 citing papers in PubMed, 14 citations in OpenAlex.
- Modulating Chikungunya and Mayaro virus-induced disease severity in mice using low concentrations of anti-IFNAR1 antibodies.Emerging microbes & infections · 2026Article
- Temporal Rewiring of Innate Immunity by Vector-Borne Viruses for Host-Directed Antiviral Therapy.International journal of molecular sciences · 2026Review
- Cell type-dependent induction of type I interferon and PARP1 activation in astrocytes and neurons during chikungunya virus infection.Microbiology spectrum · 2026Article
- Host-derived lactic acid disrupts IFN efficacy via antiviral inhibition and proinflammatory amplification.Nature communications · 2026Article
- From symptom management to immune prevention: a comprehensive review of chikungunya treatment and vaccine development.Folia microbiologica · 2026Review
- Early Immune Hypoactivation and Persistent Innate Reprogramming Characterize Chronic Chikungunya Disease.bioRxiv : the preprint server for biology · 2026Article
- IRF7 deficiency in myeloid cells results in increased disease severity and death during alphavirus encephalomyelitis despite intact expression of type I interferons.Journal of neuroinflammation · 2026Article
- Interferon-β Modulates Early Viral Replication Kinetics and Innate Responses to Non-Fatal Alphavirus Encephalomyelitis.Pathogens (Basel, Switzerland) · 2026Article
- Distinct inflammatory biomarkers associated with rheumatological outcomes in chronic chikungunya disease.Scientific reports · 2026Article
- Pathogenesis of Chronic Arthritis Due to Chikungunya Virus and Advances in Vaccine Development.Viruses · 2026Review
- Rewiring of host cell signaling in chikungunya virus infection: a mechanism for pathogenesis and therapeutic approaches.Archives of microbiology · 2026Review
- Innate immune sensing of alphavirus chikungunya: balancing antiviral defense and pathogenesis.Frontiers in immunology · 2026Review
- Hidden in Plain Sight: Alphavirus Persistence and Its Potential for Driving Chronic Pathogenesis.Viruses · 2025Review
- Phenol and chromone compounds forPharmaceutical science advances · 2025Article
- Article
- Advances and perspectives for animal models of chikungunya virus infection.Biosafety and health · 2025Review
- Novel and repurposed antiviral molecules for arbovirus infections with epidemic Potential: A systematic review.New microbes and new infections · 2025Review
- Acute Immunological Biomarkers for Predicting Chronic Rheumatologic Disease After Chikungunya Virus Infection.Tropical medicine and infectious disease · 2025Article
- Coinfection with chikungunya and Zika results in mild disease and distinct inflammatory response.Npj viruses · 2025Article
- Granulocyte colony-stimulating factor protects against acute systemic alphavirus disease in a type I IFN-dependent manner.Frontiers in immunology · 2025Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Chikungunya virus (CHIKV) is an arthritogenic alphavirus that causes both debilitating acute and chronic disease. Previous work has shown that type I interferons (IFNs) play a critical role in limiting CHIKV pathogenesis and that interferon alpha (IFN-α) and interferon beta (IFN-β) control acute CHIKV infection by distinct mechanisms. However, the role of type I IFNs, especially specific subtypes, during chronic CHIKV disease is unclear. To address this gap in knowledge, we evaluated chronic CHIKV pathogenesis in mice lacking IFN-α or IFN-β. We found that IFN-α was the dominant subtype that controls chronic disease. Despite detecting a varying type I IFN response throughout the course of disease, IFN-α acts within the first few days of infection to control the levels of persistent CHIKV RNA. In addition, using a novel CHIKV-3'-Cre tdTomato reporter system that fate maps CHIKV-infected cells, we showed that IFN-α limits the number of cells that survive CHIKV at sites of dissemination, particularly dermal fibroblasts and immune cells. Though myofibers play a significant role in CHIKV disease, they were not impacted by the loss of IFN-α. Our studies highlight that IFN-α and IFN-β play divergent roles during chronic CHIKV disease through events that occur early in infection and that not all cell types are equally dependent on type I IFNs for restricting viral persistence.
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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.