ArticlePLoS pathogens2024
Progression of herpesvirus infection remodels mitochondrial organization and metabolism.
Article in PLoS pathogens, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 15 citations in OpenAlex.
- HSV-1 metabolic hijacking: Mechanisms to precision therapeutics.Virulence · 2026Review
- Omics-guided engineering of CHO cells reveals host targets to support AAV production.Molecular therapy. Advances · 2026Article
- Herpes simplex virus 1 subverts the mitochondrial network to support the infection: A lesson on mitochondrial versatility.bioRxiv : the preprint server for biology · 2026Article
- Viral reprogramming of neuronal metabolism captured by label-free imaging in a 3D human brain tissue model.Neurophotonics · 2026Article
- Nuclear speckles are regulatory hubs for viral and host mRNA expression during HSV-1 infection.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Canine parvovirus infection affects host cell nucleolar organization and ribosome biogenesis.Communications biology · 2026Article
- Life-death trade-offs: HSV-1 ICP27 differentially modulates intrinsic apoptotic signaling in epithelial and neuron-like cells.Frontiers in microbiology · 2026Article
- Nucleus softens during herpesvirus infection.PLoS pathogens · 2026Article
- Demonstrating soft X-ray tomography in the lab for correlative cryogenic biological imaging using X-rays and light microscopy.Scientific reports · 2025Article
- HSV-1 as a Potential Driver of Alzheimer's Disease.Pathogens (Basel, Switzerland) · 2025Review
- HSV-1 hijacks mitochondrial dynamics: potential molecular mechanisms linking viral infection to neurodegenerative disorders.Apoptosis : an international journal on programmed cell death · 2025Review
- The Essential Role of Mitochondrial Dynamics in Viral Infections.International journal of molecular sciences · 2025Review
- Progression of herpesvirus infection is inhibited by calcium reporter.microPublication biology · 2024Article
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Authors and funding
26 authors at 8 institutions in 5 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Viruses target mitochondria to promote their replication, and infection-induced stress during the progression of infection leads to the regulation of antiviral defenses and mitochondrial metabolism which are opposed by counteracting viral factors. The precise structural and functional changes that underlie how mitochondria react to the infection remain largely unclear. Here we show extensive transcriptional remodeling of protein-encoding host genes involved in the respiratory chain, apoptosis, and structural organization of mitochondria as herpes simplex virus type 1 lytic infection proceeds from early to late stages of infection. High-resolution microscopy and interaction analyses unveiled infection-induced emergence of rough, thin, and elongated mitochondria relocalized to the perinuclear area, a significant increase in the number and clustering of endoplasmic reticulum-mitochondria contact sites, and thickening and shortening of mitochondrial cristae. Finally, metabolic analyses demonstrated that reactivation of ATP production is accompanied by increased mitochondrial Ca2+ content and proton leakage as the infection proceeds. Overall, the significant structural and functional changes in the mitochondria triggered by the viral invasion are tightly connected to the progression of the virus infection.
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