ArticleJournal of virology2007
The switch from latent to productive infection in epstein-barr virus-infected B cells is associated with sensitization to NK cell killing.
Article in Journal of virology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
90 citing papers in PubMed, 169 citations in OpenAlex.
- Natural killer cells against viral infection: from basic biology to immunotherapy.Precision clinical medicine · 2026Review
- Epstein-Barr virus pathogenesis and emerging control strategies.Nature reviews. Microbiology · 2025Review
- CD56Annals of hematology · 2024Article
- Entry into the lytic cycle exposes EBV-infected cells to NK cell killing via upregulation of the MICB ligand for NKG2D and activation of the CD56Frontiers in immunology · 2024Article
- Genetics of Primary Hemophagocytic Lymphohistiocytosis.Advances in experimental medicine and biology · 2024Review
- Review
- The impact of HLA polymorphism on herpesvirus infection and disease.Immunogenetics · 2023Review
- Evaluation of host cellular responses to Epstein-Barr virus (EBV) in adult lung transplant patients with EBV-associated diseases.Journal of medical virology · 2023Article
- The Role of NK Cells in EBV Infection and Related Diseases: Current Understanding and Hints for Novel Therapies.Cancers · 2023Review
- Review
- Co-Infection and Cancer: Host-Pathogen Interaction between Dendritic Cells and HIV-1, HTLV-1, and Other Oncogenic Viruses.Viruses · 2022Review
- Review
- Identification of a novel MAGT1 mutation supports a diagnosis of XMEN disease.Genes and immunity · 2022Article
- Activation and Evasion of Innate Immunity by Gammaherpesviruses.Journal of molecular biology · 2022Review
- EBV-associated diseases: Current therapeutics and emerging technologies.Frontiers in immunology · 2022Review
- Review
- Prophylactic and Therapeutic EBV Vaccines: Major Scientific Obstacles, Historical Progress, and Future Direction.Vaccines · 2021Review
- Review
- NK cells eliminate Epstein-Barr virus bound to B cells through a specific antibody-mediated uptake.PLoS pathogens · 2021Article
- Review
30 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Following activation of Epstein-Barr virus (EBV)-infected B cells from latent to productive (lytic) infection, there is a concomitant reduction in the level of cell surface major histocompatibility complex (MHC) class I molecules and an impaired antigen-presenting function that may facilitate evasion from EBV-specific CD8+ cytotoxic T cells. In some other herpesviruses studied, most notably human cytomegalovirus (HCMV), evasion of virus-specific CD8+ effector responses via downregulation of surface MHC class I molecules is supplemented with specific mechanisms for evading NK cells. We now report that EBV differs from HCMV in this respect. While latently infected EBV-positive B cells were resistant to lysis by two NK lines and by primary polyclonal NK cells from peripheral blood, these effectors efficiently killed cells activated into the lytic cycle. Susceptibility to NK lysis coincided not only with downregulation of HLA-A, -B, and -C molecules that bind to the KIR family of inhibitory receptors on NK cells but also with downregulation of HLA-E molecules binding the CD94/NKG2A inhibitory receptors. Conversely, ULBP-1 and CD112, ligands for the NK cell-activating receptors NKG2D and DNAM-1, respectively, were elevated. Susceptibility of the virus-producing target cells to NK cell lysis was partially reversed by blocking ULBP-1 or CD112 with specific antibodies. These results highlight a fundamental difference between EBV and HCMV with regards to evasion of innate immunity.
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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.