ArticlePLoS pathogens2019
The Human Cytomegalovirus UL38 protein drives mTOR-independent metabolic flux reprogramming by inhibiting TSC2.
Article in PLoS pathogens, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.
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Who cites it
50 citing papers in PubMed, 1 synthesis or guideline pooled it, 71 citations in OpenAlex.
- Prevalence of human cytomegalovirus in glioblastoma multiforme: a systematic review and meta-analysis.Journal of neuro-oncology · 2025Pooled it
- HSV-1 metabolic hijacking: Mechanisms to precision therapeutics.Virulence · 2026Review
- Article
- Glutamine supports human cytomegalovirus induced lipidome remodeling through reductive carboxylation.PLoS pathogens · 2026Article
- HCMV infection depends on EGLN1-mediated mitochondrial activation to increase dNTP pools for viral DNA replication.Cell reports · 2026Article
- 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
- Glutamine supports human cytomegalovirus induced lipidome remodeling through reductive carboxylation.bioRxiv : the preprint server for biology · 2026Article
- HCMV immediate-early protein IE2 induces neurotoxicity and hearing loss by disrupting TSC2-mTOR signaling and metabolic homeostasis.Journal of neuroinflammation · 2025Article
- Human cytomegalovirus promotesJournal of virology · 2025Article
- Herpesvirus initiation of dementias and autoimmune diseases.Journal of neurovirology · 2025Review
- Human cytomegalovirus promotesbioRxiv : the preprint server for biology · 2025Article
- Infection-induced lysine lactylation enables herpesvirus immune evasion.Science advances · 2025Article
- Metabolic hijacking styles: a review of how viral life cycles dictate glucose metabolism reprogramming.Frontiers in microbiology · 2025Review
- Viral microRNA regulation of Akt is necessary for reactivation of Human Cytomegalovirus from latency in CD34+ hematopoietic progenitor cells and humanized mice.PLoS pathogens · 2024Article
- Glucose-independent human cytomegalovirus replication is supported by metabolites that feed upper glycolytic branches.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Clinical implications of cytomegalovirus in glioblastoma progression and therapy.NPJ precision oncology · 2024Review
- Pseudorabies virus UL38 attenuates the cGAS-STING signaling pathway by recruiting Tollip to promote STING for autophagy degradation.Virology journal · 2024Article
- A UL26-PIAS1 complex antagonizes anti-viral gene expression during Human Cytomegalovirus infection.PLoS pathogens · 2024Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Human Cytomegalovirus (HCMV) infection induces several metabolic activities that are essential for viral replication. Despite the important role that this metabolic modulation plays during infection, the viral mechanisms involved are largely unclear. We find that the HCMV UL38 protein is responsible for many aspects of HCMV-mediated metabolic activation, with UL38 being necessary and sufficient to drive glycolytic activation and induce the catabolism of specific amino acids. UL38's metabolic reprogramming role is dependent on its interaction with TSC2, a tumor suppressor that inhibits mTOR signaling. Further, shRNA-mediated knockdown of TSC2 recapitulates the metabolic phenotypes associated with UL38 expression. Notably, we find that in many cases the metabolic flux activation associated with UL38 expression is largely independent of mTOR activity, as broad spectrum mTOR inhibition does not impact UL38-mediated induction of glycolysis, glutamine consumption, or the secretion of proline or alanine. In contrast, the induction of metabolite concentrations observed with UL38 expression are largely dependent on active mTOR. Collectively, our results indicate that the HCMV UL38 protein induces a pro-viral metabolic environment via inhibition of TSC2.
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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.