ArticleJournal of biochemistry2009
RNA interference targeted to the conserved dimerization initiation site (DIS) of HIV-1 restricts virus escape mutation.
Article in Journal of biochemistry, 2009. 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 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.
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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
5 citing papers in PubMed.
- Advances in HIV therapeutics and cure strategies: findings obtained through non-human primate studies.Journal of neurovirology · 2023Review
- Efficient and specific gene knockdown by small interfering RNAs produced in bacteria.Nature biotechnology · 2013Article
- Short hairpin RNAs with a 2- or 3-base mismatch inhibit HBV expression and replication in HepG2 cells.Hepatology international · 2013Article
- Arthropod-borne flaviviruses and RNA interference: seeking new approaches for antiviral therapy.Advances in virus research · 2013Review
- Antiviral Stratagems Against HIV-1 Using RNA Interference (RNAi) Technology.Evolutionary bioinformatics online · 2013Article
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Short hairpin RNAs (shRNA) targeting viral or cellular genes can effectively inhibit human immunodeficiency virus type 1 (HIV-1) replication. This inhibition, however, may induce mutations in the targeted gene, leading to rapid escape from the shRNA-induced inhibition. We generated a lymphoid cell line that stably expressed a 19-bp shRNA targeting a well-conserved dimerization initiation site (DIS) of HIV-1, which strongly inhibited viral replication, thereby delaying virus escape. Furthermore, treatment of HIV-1 infection with DIS- and vif-shRNA combination therapy resulted in superior anti-viral responses compared to vif-shRNA monotherapy. Continuous challenge with HIV-1, however, generated virus mutants that could overcome the RNA interference restriction. Such anti-genes may be promising tools for HIV-1 gene therapy for HIV/acquired immunodeficiency syndrome.
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Registered trials
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