ArticleNature communications2024
Viral modulation of type II interferon increases T cell adhesion and virus spread.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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.
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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
9 citing papers in PubMed.
- A CD54-targeted magneto-responsive nanotheranostic for precision treatment of viral pneumonia via CTSB-mediated PANoptosis inhibition.Journal of nanobiotechnology · 2026Article
- Review
- Varicella Zoster Virus Infection: Clinical Features, Molecular Pathogenesis, Treatment, and Prevention.MedComm · 2026Review
- Cancer viroimmunotherapy platforms based on varicella-zoster virus and cytomegalovirus.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Review
- Biological relevance ofMicrobiology and molecular biology reviews : MMBR · 2025Review
- Repression of varicella zoster virus gene expression during quiescent infection in the absence of detectable histone deposition.PLoS pathogens · 2025Article
- Decoding VZV's evolutionary arsenal: how Beijing strains use recombination and adaptive mutations to thrive.Virus evolution · 2025Article
- The role of viral infection in implantation failure: direct and indirect effects.Reproductive biology and endocrinology : RB&E · 2024Review
- Profiling migration of human monocytes in response to chemotactic and barotactic guidance cues.Cell reports methods · 2024Article
Corrections and comments
- Update of
Authors and funding
18 authors.
Funding
Abstract
During primary varicella zoster virus (VZV) infection, infected lymphocytes drive primary viremia, causing systemic dissemination throughout the host, including the skin. This results in cytokine expression, including interferons (IFNs), which partly limit infection. VZV also spreads from skin keratinocytes to lymphocytes prior to secondary viremia. It is not clear how VZV achieves this while evading the cytokine response. Here, we show that VZV glycoprotein C (gC) binds IFN-γ and modifies its activity, increasing the expression of a subset of IFN-stimulated genes (ISGs), including intercellular adhesion molecule 1 (ICAM1), chemokines and immunomodulatory genes. The higher ICAM1 protein level at the plasma membrane of keratinocytes facilitates lymphocyte function-associated antigen 1-dependent T cell adhesion and expression of gC during infection increases VZV spread to peripheral blood mononuclear cells. This constitutes the discovery of a strategy to modulate IFN-γ activity, upregulating a subset of ISGs, promoting enhanced lymphocyte adhesion and virus spread.
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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.