ReviewBiochemical Society transactions2020
Varicella-zoster virus: molecular controls of cell fusion-dependent pathogenesis.
Review in Biochemical Society transactions, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 24 citations in OpenAlex.
- Viral triggers of Guillain-Barré syndrome: implications for laboratory diagnostics.Biochemia medica · 2026Review
- Shingles-Like Cutaneous Manifestation of Herpes Simplex Virus Type 1 in a Young Male Patient: A Case Report.Cureus · 2026Article
- Article
- The live attenuated varicella-zoster virus vaccine vOka: Molecular and cellular biology of its skin attenuation.Human vaccines & immunotherapeutics · 2025Review
- Herpes zoster prevalence following epidural steroid injections: a retrospective review.Interventional pain medicine · 2025Article
- Post-translational modification of NK cell receptors offers clues to antigenic specificity riddle.Frontiers in immunology · 2025Review
- Oncolytic varicella-zoster virus engineered with ORF8 deletion and armed with drug-controllable interleukin-12.Journal for immunotherapy of cancer · 2024Article
- Targeted mutagenesis of the herpesvirus fusogen central helix captures transition states.Nature communications · 2023Article
- Resveratrol: a potential medication for the prevention and treatment of varicella zoster virus-induced ischemic stroke.European journal of medical research · 2023Article
- Creating the "Dew Drop on a Rose Petal": the Molecular Pathogenesis of Varicella-Zoster Virus Skin Lesions.Microbiology and molecular biology reviews : MMBR · 2023Review
- Autoimmune Heart Disease: A Comprehensive Summary for Forensic Practice.Medicina (Kaunas, Lithuania) · 2023Review
- Insights From Studies of the Genetics, Pathogenesis, and Immunogenicity of the Varicella Vaccine.The Journal of infectious diseases · 2022Article
- Review
- Review
- Dynamic Immune Landscape and VZV-Specific T Cell Responses in Patients With Herpes Zoster and Postherpetic Neuralgia.Frontiers in immunology · 2022Article
- Review
- Chicken Heat Shock Protein 70 Is an Essential Host Protein for Infectious Bursal Disease Virus Infection In Vitro.Pathogens (Basel, Switzerland) · 2021Article
- Modulation of Endosome Function, Vesicle Trafficking and Autophagy by Human Herpesviruses.Cells · 2021Review
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
Varicella-zoster virus (VZV) is the causative agent of chicken pox (varicella) and shingles (zoster). Although considered benign diseases, both varicella and zoster can cause complications. Zoster is painful and can lead to post herpetic neuralgia. VZV has also been linked to stroke, related to giant cell arteritis in some cases. Vaccines are available but the attenuated vaccine is not recommended in immunocompromised individuals and the efficacy of the glycoprotein E (gE) based subunit vaccine has not been evaluated for the prevention of varicella. A hallmark of VZV pathology is the formation of multinucleated cells termed polykaryocytes in skin lesions. This cell-cell fusion (abbreviated as cell fusion) is mediated by the VZV glycoproteins gB, gH and gL, which constitute the fusion complex of VZV, also needed for virion entry. Expression of gB, gH and gL during VZV infection and trafficking to the cell surface enables cell fusion. Recent evidence supports the concept that cellular processes are required for regulating cell fusion induced by gB/gH-gL. Mutations within the carboxyl domains of either gB or gH have profound effects on fusion regulation and dramatically restrict the ability of VZV to replicate in human skin. This loss of regulation modifies the transcriptome of VZV infected cells. Furthermore, cellular proteins have significant effects on the regulation of gB/gH-gL-mediated cell fusion and the replication of VZV, exemplified by the cellular phosphatase, calcineurin. This review provides the current state-of-the-art knowledge about the molecular controls of cell fusion-dependent pathogenesis caused by VZV.
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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.