ReviewTumour virus research2022
The oncogenic gamma herpesviruses Epstein-Barr virus (EBV) and Kaposi's sarcoma-associated herpesvirus (KSHV) hijack retinoic acid-inducible gene I (RIG-I) facilitating both viral and tumour immune evasion.
Review in Tumour virus research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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
8 citing papers in PubMed, 17 citations in OpenAlex.
- Virus-immune signatures reveal distinct clinical phenotypes and predict prognosis in patients with Kaposi's sarcoma.Journal of translational medicine · 2026Article
- Dual regulation of antiviral IFN response byJournal of pharmaceutical analysis · 2026Article
- The case for targeting latent and lytic Epstein-Barr virus infection in multiple sclerosis.Brain : a journal of neurology · 2025Review
- Immunotherapy of Oncovirus-Induced Cancers: A Review on the Development and Efficacy of Targeted Vaccines.Vaccines · 2025Review
- When viral infections meet the anti-MDA5 antibody-positive dermatomyositis.Frontiers in immunology · 2025Review
- The interplay of EBV virus and cell metabolism in lung cancer.Journal of cellular and molecular medicine · 2024Review
- Korean Chestnut Honey Suppresses HSV-1 Infection by Regulating the ROS-NLRP3 Inflammasome Pathway.Antioxidants (Basel, Switzerland) · 2023Article
- Insight into Oncogenic Viral Pathways as Drivers of Viral Cancers: Implication for Effective Therapy.Current oncology (Toronto, Ont.) · 2023Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Herpesviruses evade host immunity to establish persistent lifelong infection with dormant latent and replicative lytic phases. Epstein-Barr virus (EBV) and Kaposi's Sarcoma-associated virus (KSHV) are double-stranded DNA herpesviruses that encode components to activate RNA sensors, (Retinoic acid-inducible gene I (RIG-I) and melanoma differentiation-associated protein 5 (MDA5). Yet both viruses can effectively evade the antiviral immune response. The ability of these viruses to disarm RIG-I to evade immunity allowing viral persistency can contribute to the creation of a protected niche that facilitates tumour growth and immune evasion. Alternatively, viral nucleic acids present in the cytosol during the replicative phase of the viral lifecycle can activate pro-inflammatory signaling downstream of RIG-I augmenting tumour promoting inflammation. Understanding how these viral proteins disrupt innate immune pathways could help identify mechanisms to boost immunity, clearing viral infection and enhancing the efficacy of immunotherapy for virally induced cancers. Here we review literature on the strategies EBV and KSHV use to either enhance or inhibit RLR signaling.
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Identifiers
What OpenQuestion holds
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.