ReviewPathogens (Basel, Switzerland)2020
Herpesviral Latency-Common Themes.
Review in Pathogens (Basel, Switzerland), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
48 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Estimating the global burden of Epstein-Barr virus-related cancers.Journal of cancer research and clinical oncology · 2022Pooled it
- Virobiome-mediated regulation of microbiota-gut-brain axis signaling and neuroimmune homeostasis.Cell communication and signaling : CCS · 2026Review
- Recombinant Alphaherpesvirus Vectors in Veterinary Vaccinology: Platforms, Applications, and Translational Challenges.International journal of molecular sciences · 2026Review
- Triple Latency as a Driver of Chronic Inflammation: An Integrative View of HSV, EBV, and CMV Persistence in Immunocompetent Hosts.Clinics and practice · 2026Review
- Cross-Species Exome Sequencing Reveals Recurrent Genomic Alterations in California Sea Lion (Genes · 2026Article
- Exosome-derived miR-BART2-5p and miR-BART11-5p induced epithelial-mesenchymal transition and migration in Epstein-Barr virus-associated gastric carcinoma.Journal of molecular histology · 2026Article
- Article
- Bat things come in threes: within-host dynamics of herpesvirus triple infection in bats.Journal of virology · 2025Article
- Chronic Neuroplasticity Changes Following Neurotropic Viral Infection: Mechanisms and Implications.Cellular and molecular neurobiology · 2025Review
- Functional and Structural Determinants of Long- and Short-Term Evolution of Herpesvirus Proteins.Molecular biology and evolution · 2025Article
- The Involvement of Herpesviruses in the Pathogenesis of Thoracic Aortic Aneurysms: Passive Bystanders or Active Contributors?Reviews in cardiovascular medicine · 2025Review
- Protein Language Models Expose Viral Immune Mimicry.Viruses · 2025Article
- Review
- Reactivation of Latent Tuberculosis Following COVID-19 and Epstein-Barr Virus Coinfection: A Case Report.Pathogens (Basel, Switzerland) · 2025Article
- Development and validation of a novel triplex droplet digital PCR assay for simultaneous detection of African swine fever virus, pseudorabies virus, and porcine parvovirus.Frontiers in microbiology · 2025Article
- Peripheral B Lymphocyte Serves as a Reservoir for the Persistently Covert Infection of Mandarin FishViruses · 2024Article
- Hypoxic reactivation of Kaposi's sarcoma associated herpesvirus.Cell insight · 2024Review
- Bovine Gammaherpesvirus 6 Tropism in the Natural Host.Viruses · 2024Article
- Sequence analysis of isolated strains of herpes zoster virus among patients with shingles.Iranian journal of microbiology · 2024Article
- Cytomegalovirus, Epstein-Barr Virus, Herpes Simplex Virus, and Varicella Zoster Virus Infection Dynamics in People with Multiple Sclerosis from Northern Italy.Pathogens (Basel, Switzerland) · 2024Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
Latency establishment is the hallmark feature of herpesviruses, a group of viruses, of which nine are known to infect humans. They have co-evolved alongside their hosts, and mastered manipulation of cellular pathways and tweaking various processes to their advantage. As a result, they are very well adapted to persistence. The members of the three subfamilies belonging to the family Herpesviridae differ with regard to cell tropism, target cells for the latent reservoir, and characteristics of the infection. The mechanisms governing the latent state also seem quite different. Our knowledge about latency is most complete for the gammaherpesviruses due to previously missing adequate latency models for the alpha and beta-herpesviruses. Nevertheless, with advances in cell biology and the availability of appropriate cell-culture and animal models, the common features of the latency in the different subfamilies began to emerge. Three criteria have been set forth to define latency and differentiate it from persistent or abortive infection: 1) persistence of the viral genome, 2) limited viral gene expression with no viral particle production, and 3) the ability to reactivate to a lytic cycle. This review discusses these criteria for each of the subfamilies and highlights the common strategies adopted by herpesviruses to establish latency.
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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.