ArticleScientific reports2016
Peroxisomes are platforms for cytomegalovirus' evasion from the cellular immune response.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
What it found
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Who cites it
36 citing papers in PubMed, 54 citations in OpenAlex.
- PEX19 restricts porcine deltacoronavirus replication through farnesylation-dependent and -independent mechanisms.Journal of virology · 2026Article
- MAVS oligomerization drives a faster and more efficient antiviral signaling activation at peroxisomes compared to mitochondria.The FEBS journal · 2026Article
- Remodeling of Metabolic and Secretory Organelles During Oncogenic and Oncomodulatory Viral Infections.Viruses · 2026Review
- Article
- Protein Kinase C promotes peroxisome biogenesis and peroxisome-endoplasmic reticulum interaction.The Journal of cell biology · 2025Article
- Shaping Viral Infection Outcomes via Organelle Remodeling.Annual review of virology · 2025Review
- Macrophage peroxisomes guide alveolar regeneration and limit SARS-CoV-2 tissue sequelae.Science (New York, N.Y.) · 2025Article
- Peroxisomes as emerging clinical targets in neuroinflammatory diseases.Frontiers in molecular neuroscience · 2025Review
- HCMV strain- and cell type-specific alterations in membrane contact sites point to the convergent regulation of organelle remodeling.Journal of virology · 2024Article
- Article
- No Time to Die: How Cytomegaloviruses Suppress Apoptosis, Necroptosis, and Pyroptosis.Viruses · 2024Review
- Article
- A Cysteine Residue of Human Cytomegalovirus vMIA Protein Plays a Crucial Role in Viperin Trafficking to Control Viral Infectivity.Journal of virology · 2023Article
- Peroxisomes and Viruses: Overview on Current Knowledge and Experimental Approaches.Methods in molecular biology (Clifton, N.J.) · 2023Review
- Restructured membrane contacts rewire organelles for human cytomegalovirus infection.Nature communications · 2022Article
- Virus-host protein interactions as footprints of human cytomegalovirus replication.Current opinion in virology · 2022Review
- Article
- Human Cytomegalovirus vMIA Inhibits MAVS Oligomerization at Peroxisomes in an MFF-Dependent Manner.Frontiers in cell and developmental biology · 2022Article
- Review
- Viperin interacts with PEX19 to mediate peroxisomal augmentation of the innate antiviral response.Life science alliance · 2021Article
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 4 countries.
Funding
Abstract
The human cytomegalovirus developed distinct evasion mechanisms from the cellular antiviral response involving vMIA, a virally-encoded protein that is not only able to prevent cellular apoptosis but also to inhibit signalling downstream from mitochondrial MAVS. vMIA has been shown to localize at mitochondria and to trigger their fragmentation, a phenomenon proven to be essential for the signalling inhibition. Here, we demonstrate that vMIA is also localized at peroxisomes, induces their fragmentation and inhibits the peroxisomal-dependent antiviral signalling pathway. Importantly, we demonstrate that peroxisomal fragmentation is not essential for vMIA to specifically inhibit signalling downstream the peroxisomal MAVS. We also show that vMIA interacts with the cytoplasmic chaperone Pex19, suggesting that the virus has developed a strategy to highjack the peroxisomal membrane proteins' transport machinery. Furthermore, we show that vMIA is able to specifically interact with the peroxisomal MAVS. Our results demonstrate that peroxisomes constitute a platform for evasion of the cellular antiviral response and that the human cytomegalovirus has developed a mechanism by which it is able to specifically evade the peroxisomal MAVS-dependent antiviral signalling.
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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.