ArticleNucleic acids research2009
RNAi-mediated inhibition of HIV-1 by targeting partially complementary viral sequences.
Article in Nucleic acids research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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
10 citing papers in PubMed, 27 citations in OpenAlex.
- Anti-inflammatory effects of miR-150 are associated with the downregulation of STAT1 in macrophages following lipopolysaccharide treatment.Experimental and therapeutic medicine · 2021Article
- Biogenesis, evolution and functional targets of microRNA-125a.Molecular genetics and genomics : MGG · 2013Review
- Selection of RNAi-based inhibitors for anti-HIV gene therapy.World journal of virology · 2012Review
- Antiviral RNAi: translating science towards therapeutic success.Pharmaceutical research · 2011Review
- Targeted delivery of mutant tolerant anti-coxsackievirus artificial microRNAs using folate conjugated bacteriophage Phi29 pRNA.PloS one · 2011Article
- An RNAi in silico approach to find an optimal shRNA cocktail against HIV-1.Virology journal · 2010Article
- Absence of DICER in monocytes and its regulation by HIV-1.The Journal of biological chemistry · 2010Article
- Titers of lentiviral vectors encoding shRNAs and miRNAs are reduced by different mechanisms that require distinct repair strategies.RNA (New York, N.Y.) · 2010Article
- Anticipating and blocking HIV-1 escape by second generation antiviral shRNAs.Retrovirology · 2010Article
- Changes in the Plasticity of HIV-1 Nef RNA during the Evolution of the North American Epidemic.PloS oneArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Potent antiviral RNAi can be induced by intracellular expression of short hairpin RNAs (shRNAs) and artificial microRNAs (miRNAs). Expression of shRNA and miRNA results in target mRNA degradation (perfect base pairing) or translational repression (partial base pairing). Although efficient inhibition can be obtained, error-prone viruses such as human immunodeficiency virus type 1 (HIV-1) can escape from RNAi-mediated inhibition by mutating the target sequence. Recently, artificial miRNAs have been shown to be potent RNAi inducers due to their efficient processing by the RNAi machinery. Furthermore, miRNAs may be more proficient in suppressing imperfect targets than shRNAs. In this study, we tested the knockdown efficiency of miRNAs and shRNAs against wild-type and RNAi-escape HIV-1 variants with one or two mutations in the target sequence. ShRNAs and miRNAs can significantly inhibit the production of HIV-1 variants with mutated target sequences in the open reading frame. More pronounced mutation-tolerance was measured for targets in the 3' untranslated region (3' UTR). Partially complementary sequences within the 3' UTR of the HIV-1 RNA genome efficiently act as target sites for miRNAs and shRNAs. These data suggest that targeting imperfect target sites by antiviral miRNAs or shRNAs provides an alternative RNAi approach for inhibition of pathogenic viruses.
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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.