ArticlePloS one2017
Epstein-Barr virus infection-induced inflammasome activation in human monocytes.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 51 citations in OpenAlex.
- Epstein Barr Virus Infection Affects Function of Cytotoxic T Lymphocytes in Patients with Severe Aplastic Anemia.BioMed research international · 2018Trial
- HIGH DOSE GAMMAHERPESVIRUS INFECTION IN MACROPHAGES RESULTS IN INFLAMMATORY MULTIMODAL CELL DEATH.bioRxiv : the preprint server for biology · 2026Article
- AIM2-mediated pyroptosis correlates with viral load and liver injury in children with primary Epstein-Barr virus infection.BMC pediatrics · 2026Article
- Epstein-Barr virus infection exacerbates ulcerative colitis by driving macrophage pyroptosis via the upregulation of glycolysis.Precision clinical medicine · 2025Article
- Activation and evasion of inflammasomes during viral and microbial infection.Cellular and molecular life sciences : CMLS · 2025Review
- Catch me if you can: viral nucleic acids to host sensors.Frontiers in immunology · 2025Review
- Review
- Barrier-to-autointegration factor 1 promotes gammaherpesvirus reactivation from latency.Nature communications · 2023Article
- The innate and T-cell mediated immune response during acute and chronic gammaherpesvirus infection.Frontiers in cellular and infection microbiology · 2023Review
- Context-dependent functions of pattern recognition receptors in cancer.Nature reviews. Cancer · 2022Review
- Review
- BRLF1 suppresses RNA Pol III-mediated RIG-I inflammasome activation in the early EBV lytic lifecycle.EMBO reports · 2021Article
- Activation and Immune Regulation Mechanisms of PYHIN Family During Microbial Infection.Frontiers in microbiology · 2021Review
- Interplays between inflammasomes and viruses, bacteria (pathogenic and probiotic), yeasts and parasites.Immunology letters · 2020Review
- Immunobiology and structural biology of AIM2 inflammasome.Molecular aspects of medicine · 2020Review
- AIM2 in health and disease: Inflammasome and beyond.Immunological reviews · 2020Review
- A promiscuous inflammasome sparks replication of a common tumor virus.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- HPV E7 inhibits cell pyroptosis by promoting TRIM21-mediated degradation and ubiquitination of the IFI16 inflammasome.International journal of biological sciences · 2020Article
- Role of AIM2 inflammasome in inflammatory diseases, cancer and infection.European journal of immunology · 2019Review
- Epstein-Barr Virus and Innate Immunity: Friends or Foes?Microorganisms · 2019Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammasomes are cytoplasmic sensors that regulate the activity of caspase-1 and the secretion of interleukin-1β (IL-1β) or interleukin-18 (IL-18) in response to foreign molecules, including viral pathogens. They are considered to be an important link between the innate and adaptive immune responses. However, the mechanism by which inflammasome activation occurs during primary Epstein-Barr virus (EBV) infection remains unknown. Human B lymphocytes and epithelial cells are major targets of EBV, although it can also infect a variety of other cell types. In this study, we found that EBV could infect primary human monocytes and the monocyte cell line, THP-1, inducing inflammasome activation. We incubated cell-free EBV with THP-1 cells or primary human monocytes, then confirmed EBV infection using confocal microscopy and flow cytometry. Lytic and latent EBV genes were detected by real-time RT-PCR in EBV-infected monocytes. EBV infection of THP-1 cells and primary human monocytes induced caspase-dependent IL-1β production, while EBV infection of B-cell or T-cell lines did not induce IL-1β production. To identify the sensor molecule responsible for inflammasome activation during EBV infection, we examined the mRNA and the protein levels of NLR family pyrin domain-containing 3 (NLRP3), absent in melanoma 2 (AIM2), and interferon-inducible protein 16 (IFI16). Increased AIM2 levels were observed in EBV-infected THP-1 cells and primary human monocytes, whereas levels of IFI16 and NLRP3 did not show remarkable change. Furthermore, knockdown of AIM2 by small interfering RNA attenuated caspase-1 activation. Taken together, our results suggest that EBV infection of human monocytes induces caspase-1-dependent IL-1β production, and that AIM2, acting as an inflammasome, is involved in this response.
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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.