ArticleCell reports2024
Poxvirus A51R proteins regulate microtubule stability and antagonize a cell-intrinsic antiviral response.
Article in Cell reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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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Who cites it
7 citing papers in PubMed, 8 citations in OpenAlex.
- Mammalian innate antiviral defenses: beyond interferon.Journal of virology · 2025Review
- Vaccinia virus modulates the redox environment by inhibiting reactive oxygen and nitrogen species with increased activity of endogenous antioxidant enzymes.Scientific reports · 2025Article
- Temporal expression classes and functions of vaccinia virus and mpox (monkeypox) virus genes.mBio · 2025Review
- TRIM Proteins and Antiviral Microtubule Reorganization: A Novel Component in Innate Immune Responses?Viruses · 2024Review
- Poxvirus A51R Proteins Negatively Regulate Microtubule-Dependent Transport by Kinesin-1.International journal of molecular sciences · 2024Article
- Monkeypox: A Viral Zoonotic Disease of Rising Global Concern.Infectious diseases & immunity · 2024Review
- FEAR antiviral response pathway is independent of interferons and countered by poxvirus proteins.Nature microbiology · 2024Article
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Numerous viruses alter host microtubule (MT) networks during infection, but how and why they induce these changes is unclear in many cases. We show that the vaccinia virus (VV)-encoded A51R protein is a MT-associated protein (MAP) that directly binds MTs and stabilizes them by both promoting their growth and preventing their depolymerization. Furthermore, we demonstrate that A51R-MT interactions are conserved across A51R proteins from multiple poxvirus genera, and highly conserved, positively charged residues in A51R proteins mediate these interactions. Strikingly, we find that viruses encoding MT interaction-deficient A51R proteins fail to suppress a reactive oxygen species (ROS)-dependent antiviral response in macrophages that leads to a block in virion morphogenesis. Moreover, A51R-MT interactions are required for VV virulence in mice. Collectively, our data show that poxviral MAP-MT interactions overcome a cell-intrinsic antiviral ROS response in macrophages that would otherwise block virus morphogenesis and replication in animals.
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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.