ArticlePloS one2010
Epstein-Barr virus interferes with the amplification of IFNalpha secretion by activating suppressor of cytokine signaling 3 in primary human monocytes.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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.
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Who cites it
31 citing papers in PubMed, 47 citations in OpenAlex.
- Gene Expression of Suppressor of Cytokine Signaling 3 (SOCS3), Interferons Alpha and Beta (IFN-α and β) in Common Warts.Indian dermatology online journal · 2026Article
- EBV Early Lytic Antigens, EBNA2 and PDL-1, in Progressive Multiple Sclerosis Brain: A Coordinated Contribution to Viral Immune Evasion.International journal of molecular sciences · 2025Article
- SOCS Proteins: Key Players in Immune Regulation During SARS-CoV-2 Infection.European journal of immunology · 2025Review
- Epstein-Barr virus: the mastermind of immune chaos.Frontiers in immunology · 2024Review
- Epstein-Barr virus infection: the micro and macro worlds.Virology journal · 2023Review
- Comprehensive insight into altered host cell-signaling cascades upon Helicobacter pylori and Epstein-Barr virus infections in cancer.Archives of microbiology · 2023Review
- Negative regulation of type I interferon signaling by integrin-linked kinase permits dengue virus replication.PLoS pathogens · 2023Article
- The innate and T-cell mediated immune response during acute and chronic gammaherpesvirus infection.Frontiers in cellular and infection microbiology · 2023Review
- Mechanisms contributing to adverse outcomes of COVID-19 in obesity.Molecular and cellular biochemistry · 2022Review
- Activation and Evasion of Innate Immunity by Gammaherpesviruses.Journal of molecular biology · 2022Review
- Mechanism of herpesvirus protein kinase UL13 in immune escape and viral replication.Frontiers in immunology · 2022Review
- EBV Infection and Its Regulated Metabolic Reprogramming in Nasopharyngeal Tumorigenesis.Frontiers in cellular and infection microbiology · 2022Review
- Review
- Oncogenic Viruses as Entropic Drivers of Cancer Evolution.Frontiers in virology (Lausanne, Switzerland) · 2021Article
- Virus-Induced Tumorigenesis and IFN System.Biology · 2021Review
- Role of Leptin in Inflammation and Vice Versa.International journal of molecular sciences · 2020Review
- SOCS Proteins Participate in the Regulation of Innate Immune Response Caused by Viruses.Frontiers in immunology · 2020Review
- Epstein-Barr Virus and Innate Immunity: Friends or Foes?Microorganisms · 2019Review
- Manipulation of Type I Interferon Signaling by HIV and AIDS-Associated Viruses.Journal of immunology research · 2019Review
- SOCS and Herpesviruses, With Emphasis on Cytomegalovirus Retinitis.Frontiers in immunology · 2019Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundEpstein-Barr virus is recognized to cause lymphoproliferative disorders and is also associated with cancer. Evidence suggests that monocytes are likely to be involved in EBV pathogenesis, especially due to a number of cellular functions altered in EBV-infected monocytes, a process that may affect efficient host defense. Because type I interferons (IFNs) are crucial mediators of host defense against viruses, we investigated the effect of EBV infection on the IFNalpha pathway in primary human monocytes. METHODOLOGY/PRINCIPAL
findingsInfection of monocytes with EBV induced IFNalpha secretion but inhibited the positive feedback loop for the amplification of IFNalpha. We showed that EBV infection induced the expression of suppressor of cytokine signaling 3 (SOCS3) and, to a lesser extent, SOCS1, two proteins known to interfere with the amplification of IFNalpha secretion mediated by the JAK/STAT signal transduction pathway. EBV infection correlated with a blockage in the activation of JAK/STAT pathway members and affected the level of phosphorylated IFN regulatory factor 7 (IRF7). Depletion of SOCS3, but not SOCS1, by small interfering RNA (siRNA) abrogated the inhibitory effect of EBV on JAK/STAT pathway activation and significantly restored IFNalpha secretion. Finally, transfection of monocytes with the viral protein Zta caused the upregulation of SOCS3, an event that could not be recapitulated with mutated Zta. CONCLUSIONS/SIGNIFICANCE: We propose that EBV protein Zta activates SOCS3 protein as an immune escape mechanism that both suppresses optimal IFNalpha secretion by human monocytes and favors a state of type I IFN irresponsiveness in these cells. This immunomodulatory effect is important to better understand the aspects of the immune response to EBV.
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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.