ArticleProceedings of the National Academy of Sciences of the United States of America2021
The human cytomegalovirus protein pUL13 targets mitochondrial cristae architecture to increase cellular respiration during infection.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed.
- Glutamine supports human cytomegalovirus induced lipidome remodeling through reductive carboxylation.PLoS pathogens · 2026Article
- Review
- Cristae: bridging bioenergetic hubs and compartmental barriers in mitochondrial homeostasis.Cell death & disease · 2026Review
- Remodeling of Metabolic and Secretory Organelles During Oncogenic and Oncomodulatory Viral Infections.Viruses · 2026Review
- Emerging approaches for characterizing spatial and temporal dynamics of pathogen-induced organelle remodeling.Cell systems · 2026Review
- Metabolic hijackers: how viral proteins redefine host cell landscapes.Journal of virology · 2026Review
- Does human cytomegalovirus provide a novel therapeutic target for patients with glioblastoma?Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025Review
- Human cytomegalovirus promotesJournal of virology · 2025Article
- Shaping Viral Infection Outcomes via Organelle Remodeling.Annual review of virology · 2025Review
- Article
- Human cytomegalovirus promotesbioRxiv : the preprint server for biology · 2025Article
- Alzheimer's disease-associated CD83(+) microglia are linked with increased immunoglobulin G4 and human cytomegalovirus in the gut, vagal nerve, and brain.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Human cytomegalovirus: pathogenesis, prevention, and treatment.Molecular biomedicine · 2024Review
- HCMV strain- and cell type-specific alterations in membrane contact sites point to the convergent regulation of organelle remodeling.Journal of virology · 2024Article
- Insights into the Role of VPS39 and Its Interaction with CP204L and A137R in ASFV Infection.Viruses · 2024Article
- Progression of herpesvirus infection remodels mitochondrial organization and metabolism.PLoS pathogens · 2024Article
- Tapioca: a platform for predicting de novo protein-protein interactions in dynamic contexts.Nature methods · 2024Article
- Intermittent cytomegalovirus infection alters neurobiological metabolism and induces cognitive deficits in mice.Brain, behavior, and immunity · 2024Article
- Review
- Role of immunometabolism during congenital cytomegalovirus infection.Immunometabolism (Cobham, Surrey) · 2023Article
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Authors and funding
7 authors.
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Abstract
Viruses modulate mitochondrial processes during infection to increase biosynthetic precursors and energy output, fueling virus replication. In a surprising fashion, although it triggers mitochondrial fragmentation, the prevalent pathogen human cytomegalovirus (HCMV) increases mitochondrial metabolism through a yet-unknown mechanism. Here, we integrate molecular virology, metabolic assays, quantitative proteomics, and superresolution confocal microscopy to define this mechanism. We establish that the previously uncharacterized viral protein pUL13 is required for productive HCMV replication, targets the mitochondria, and functions to increase oxidative phosphorylation during infection. We demonstrate that pUL13 forms temporally tuned interactions with the mitochondrial contact site and cristae organizing system (MICOS) complex, a critical regulator of cristae architecture and electron transport chain (ETC) function. Stimulated emission depletion superresolution microscopy shows that expression of pUL13 alters cristae architecture. Indeed, using live-cell Seahorse assays, we establish that pUL13 alone is sufficient to increase cellular respiration, not requiring the presence of other viral proteins. Our findings address the outstanding question of how HCMV targets mitochondria to increase bioenergetic output and expands the knowledge of the intricate connection between mitochondrial architecture and ETC function.
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