ArticleNature communications2024
Human cytomegalovirus harnesses host L1 retrotransposon for efficient replication.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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The trial behind it
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Who cites it
5 citing papers in PubMed.
- LINE-1 transposable element is expressed in Kaposi's sarcoma and regulates gene expression in KSHV-infected cells.bioRxiv : the preprint server for biology · 2026Article
- A Review of Current Computational Tools for Peptide-Protein Docking.Journal of computational chemistry · 2026Review
- Antagonistic co-evolution throughout the herpesvirus life cycle.Virus evolution · 2026Review
- Human cytomegalovirus infection induces L1 expression through UL38-dependent mTOR-KAP1 pathway.PloS one · 2025Article
- Recent advances in human cytomegalovirus: a comprehensive review of pathogenic mechanisms, virus-host interactions, and antiviral strategies.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
15 authors.
Funding
Abstract
Genetic parasites, including viruses and transposons, exploit components from the host for their own replication. However, little is known about virus-transposon interactions within host cells. Here, we discover a strategy where human cytomegalovirus (HCMV) hijacks L1 retrotransposon encoded protein during its replication cycle. HCMV infection upregulates L1 expression by enhancing both the expression of L1-activating transcription factors, YY1 and RUNX3, and the chromatin accessibility of L1 promoter regions. Increased L1 expression, in turn, promotes HCMV replicative fitness. Affinity proteomics reveals UL44, HCMV DNA polymerase subunit, as the most abundant viral binding protein of the L1 ribonucleoprotein (RNP) complex. UL44 directly interacts with L1 ORF2p, inducing DNA damage responses in replicating HCMV compartments. While increased L1-induced mutagenesis is not observed in HCMV for genetic adaptation, the interplay between UL44 and ORF2p accelerates viral DNA replication by alleviating replication stress. Our findings shed light on how HCMV exploits host retrotransposons for enhanced viral fitness.
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