Trial reportPLoS pathogens2014
RNA-seq analysis of host and viral gene expression highlights interaction between varicella zoster virus and keratinocyte differentiation.
Trial report in PLoS pathogens, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 51 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
51 citing papers in PubMed, 73 citations in OpenAlex.
- Varicella zoster virus infection.Nature reviews. Disease primers · 2026Review
- Low-Level Light Therapy in Postherpetic Neuralgia: A Review of Mechanistic Insights and Clinical Implications.Cellular and molecular neurobiology · 2026Review
- Comparative analysis of varicella-zoster virus and herpes simplex virus 1 interaction with epidermal terminal differentiation in primary human keratinocytes models of differentiation.bioRxiv : the preprint server for biology · 2026Article
- Targeting Host Metabolic and Epigenetic Rewiring Blocks Lytic Gammaherpesvirus Production.Viruses · 2026Article
- The live attenuated varicella-zoster virus vaccine vOka: Molecular and cellular biology of its skin attenuation.Human vaccines & immunotherapeutics · 2025Review
- Nasal mucus-derived KLK13 restricts SARS-CoV-2 infection via proteolytic cleavage of spike.mBio · 2025Article
- Biological relevance ofMicrobiology and molecular biology reviews : MMBR · 2025Review
- Marek's disease virus replication in chicken skin reconstructedThe Journal of general virology · 2025Article
- Generation of theInternational journal of molecular sciences · 2025Article
- Upregulation of keratin 15 is required for varicella-zoster virus replication in keratinocytes and is attenuated in the live attenuated vOka vaccine strain.Virology journal · 2024Article
- Commercial human 3D corneal epithelial equivalents for modeling epithelial infection in herpes keratitis.Virology · 2024Article
- Review
- Creating the "Dew Drop on a Rose Petal": the Molecular Pathogenesis of Varicella-Zoster Virus Skin Lesions.Microbiology and molecular biology reviews : MMBR · 2023Review
- Stage of Keratinocyte Differentiation Is a Key Determinant of Viral Susceptibility in Human Skin.The Journal of investigative dermatology · 2023Article
- Article
- Review
- Article
- Development of a skin- and neuro-attenuated live vaccine for varicella.Nature communications · 2022Article
- Genome-wide transcriptome analysis of porcine epidemic diarrhea virus virulent or avirulent strain-infected porcine small intestinal epithelial cells.Virologica Sinica · 2022Article
- Characterization of plasma metabolites and proteins in patients with herpetic neuralgia and development of machine learning predictive models based on metabolomic profiling.Frontiers in molecular neuroscience · 2022Article
Corrections and comments
- Erratum issued
Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
Abstract
Varicella zoster virus (VZV) is the etiological agent of chickenpox and shingles, diseases characterized by epidermal skin blistering. Using a calcium-induced keratinocyte differentiation model we investigated the interaction between epidermal differentiation and VZV infection. RNA-seq analysis showed that VZV infection has a profound effect on differentiating keratinocytes, altering the normal process of epidermal gene expression to generate a signature that resembles patterns of gene expression seen in both heritable and acquired skin-blistering disorders. Further investigation by real-time PCR, protein analysis and electron microscopy revealed that VZV specifically reduced expression of specific suprabasal cytokeratins and desmosomal proteins, leading to disruption of epidermal structure and function. These changes were accompanied by an upregulation of kallikreins and serine proteases. Taken together VZV infection promotes blistering and desquamation of the epidermis, both of which are necessary to the viral spread and pathogenesis. At the same time, analysis of the viral transcriptome provided evidence that VZV gene expression was significantly increased following calcium treatment of keratinocytes. Using reporter viruses and immunohistochemistry we confirmed that VZV gene and protein expression in skin is linked with cellular differentiation. These studies highlight the intimate host-pathogen interaction following VZV infection of skin and provide insight into the mechanisms by which VZV remodels the epidermal environment to promote its own replication and spread.
Indexed as
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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.