ArticleBiology2024
RETRACTED: IAV Antagonizes Host Innate Immunity by Weakening the LncRNA-LRIR2-Mediated Antiviral Functions.
Article in Biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 1 paper.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Article
Corrections and comments
- Retracted
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A growing number of studies have shown that long non-coding RNAs (lncRNAs) are implicated in many biological processes, including the regulation of innate immunity and IAV replication. In addition, IAV has been found to be able to hijack lncRNAs and thus antagonize host innate immunity. Nonetheless, whether IAV can antagonize host innate immunity by weakening the antiviral functions mediated by lncRNAs is unknown. In this study, we found that LncRNA-ENST00000491430 regulates IAV replication and named it LRIR2. Interestingly, we found that the expression of LRIR2 was suppressed during IAV infection. Importantly, LRIR2 overexpression inhibited IAV replication, suggesting that LRIR2 plays an antiviral role during IAV infection. Mechanistically, we demonstrated that LRIR2 inhibits the transcription and replication of the IAV genome. In addition, the antiviral function of LRIR2 is mainly dependent on the stem-loop structures of 1-118 nt and 575-683 nt. Taken together, IAV could antagonize host innate immunity by weakening the LncRNA-LRIR2-mediated antiviral functions. Our study provides novel perspectives into viral strategies to antagonize host innate immunity. It lays a theoretical foundation for the design of novel anti-IAV drugs that target host lncRNAs or the antagonism effect.
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Registered trials
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