ArticleNature microbiology2025
Human cytomegalovirus long non-coding RNA counteracts nuclear cGAS to facilitate immune evasion.
Article in Nature microbiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed.
- The Janus face of host LncRNA in viral infections: Defender or collaborator?Communications biology · 2026Review
- HIV infection reprogrammes CD4+ T cells for quiescence and entry into proviral latency.Nature microbiology · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors.
Funding
Abstract
Viruses have evolved diverse immune evasion strategies, including the targeting of host pattern recognition receptors. The role of viral non-coding RNAs in modulating pattern recognition receptor activity is unclear. Here we show that human cytomegalovirus (HCMV) produces long non-coding RNA4.9 that counteracts the nuclear cyclic GMP-AMP synthase (cGAS)-mediated immune response to facilitate viral infection in human foreskin fibroblasts. RNA4.9 interacts with host cGAS via its 75-nucleotide RNA region with predicted hairpin loops. Binding of RNA4.9 to cGAS inhibits cGAS enzymatic activity as well as downstream interferon response and facilitates productive viral replication. Sterically blocking the folding of the 75-nucleotide region with antisense oligonucleotides during HCMV infection restores cGAS activity and impairs viral replication. In addition, we found that the specific localization of RNA4.9, which concentrates near HCMV DNA, is correlated with its efficient binding to cGAS and subsequent immune suppression. Our findings identify viral non-coding RNAs as key regulators of cGAS and highlight their potential as therapeutic targets.
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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.