ArticleFrontiers in immunology2024
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 CD56
Article in Frontiers in immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- The case for an Epstein-Barr virus vaccine: Lessons from its link to systemic lupus erythematosus.Human vaccines & immunotherapeutics · 2026Review
- Natural killer cells against viral infection: from basic biology to immunotherapy.Precision clinical medicine · 2026Review
- A BRRF1-CCR4-NOT axis underlies conserved transcriptome-wide loss of splicing fidelity during gammaherpesvirus reactivation.bioRxiv : the preprint server for biology · 2026Article
- Recent advances in Epstein-Barr virus vaccines development from mechanistic exploration to clinical translation.NPJ vaccines · 2026Review
- Killer cell immunoglobulin-like receptor (KIR) alleles suggested to be associated with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS).Brain, behavior, and immunity · 2025Article
- Targeting archetypes of viral-driven cancers with immunotherapy: a perspective on immunogenicity within the tumor microenvironment.Frontiers in immunology · 2025Review
- T cell-mediated immune surveillance conferred by latent Epstein-Barr virus genes suppresses a broad spectrum of tumor formation through NKG2D-NKG2DL interactions.Frontiers in immunology · 2025Article
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Epstein-Barr virus (EBV) is usually acquired during infancy as an asymptomatic infection and persists throughout life in a latent state under the control of the host immune system. However, EBV is associated with various malignant diseases that preferentially develop in immunodeficient individuals. Accumulating evidence suggests an important role for NK cells, though the mechanisms by which EBV evades or triggers NK cell responses are poorly understood. Here, we generated EBV-immortalized lymphoblastoid cell lines stably expressing an inducible form of the BZLF1 early lytic viral protein (LCL-Z) to challenge primary NK cells with EBV
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