ArticleNature communications2023
The poxvirus F17 protein counteracts mitochondrially orchestrated antiviral responses.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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.
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
17 citing papers in PubMed, 19 citations in OpenAlex.
- The factory enters the fray: how mitochondrial protein trafficking shapes the host response to infection.Journal of virology · 2026Review
- Molecular mechanism of 2',3'-cGAMP degradation by monkeypox virus poxin-schlafen protein.The Journal of biological chemistry · 2026Article
- Review
- Viral-host interactions mediated by the mTOR signaling pathway.Cell insight · 2026Review
- Metabolic hijackers: how viral proteins redefine host cell landscapes.Journal of virology · 2026Review
- Mpox virus poxin-schlafen fusion protein suppresses innate antiviral response by sequestering STAT2.Emerging microbes & infections · 2025Article
- Lumpy Skin Disease Virus Pathogenesis: Viral Protein Functions and Comparative Insights from Vaccinia Virus.Animals : an open access journal from MDPI · 2025Review
- Vaccinia virus modulates the redox environment by inhibiting reactive oxygen and nitrogen species with increased activity of endogenous antioxidant enzymes.Scientific reports · 2025Article
- Distinct non-canonical translation initiation modes arise for specific host and viral mRNAs during poxvirus-induced shutoff.Nature microbiology · 2025Article
- Temporal expression classes and functions of vaccinia virus and mpox (monkeypox) virus genes.mBio · 2025Review
- Ribosome customization and functional diversification among P-stalk proteins regulate late poxvirus protein synthesis.Cell reports · 2025Article
- Orthoflavivirus infection and the mTOR signaling pathway.Frontiers in microbiology · 2025Review
- Mpox-Induced Metabolic Alterations.Journal of cellular and molecular medicine · 2025Review
- STING exerts antiviral innate immune response by activating pentose phosphate pathway.Cell communication and signaling : CCS · 2024Article
- Metabolic reprogramming tips vaccinia virus infection outcomes by stabilizing interferon-γ induced IRF1.PLoS pathogens · 2024Article
- Poxin-deficient poxviruses are sensed by cGAS prior to genome replication.The Journal of general virology · 2024Article
- Vaccinia virus Tiantan strain blocks host antiviral innate immunity and programmed cell death by disrupting gene expression.Biosafety and health · 2024Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Poxviruses are unusual DNA viruses that replicate in the cytoplasm. To do so, they encode approximately 100 immunomodulatory proteins that counteract cytosolic nucleic acid sensors such as cGAMP synthase (cGAS) along with several other antiviral response pathways. Yet most of these immunomodulators are expressed very early in infection while many are variable host range determinants, and significant gaps remain in our understanding of poxvirus sensing and evasion strategies. Here, we show that after infection is established, subsequent progression of the viral lifecycle is sensed through specific changes to mitochondria that coordinate distinct aspects of the antiviral response. Unlike other viruses that cause extensive mitochondrial damage, poxviruses sustain key mitochondrial functions including membrane potential and respiration while reducing reactive oxygen species that drive inflammation. However, poxvirus replication induces mitochondrial hyperfusion that independently controls the release of mitochondrial DNA (mtDNA) to prime nucleic acid sensors and enables an increase in glycolysis that is necessary to support interferon stimulated gene (ISG) production. To counter this, the poxvirus F17 protein localizes to mitochondria and dysregulates mTOR to simultaneously destabilize cGAS and block increases in glycolysis. Our findings reveal how the poxvirus F17 protein disarms specific mitochondrially orchestrated responses to later stages of poxvirus replication.
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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.