ArticleCell host & microbe2008
HIV evades RNA interference directed at TAR by an indirect compensatory mechanism.
Article in Cell host & microbe, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed, 43 citations in OpenAlex.
- Article
- Insights Into Persistent HIV-1 Infection and Functional Cure: Novel Capabilities and Strategies.Frontiers in microbiology · 2022Review
- The role of exosomal transport of viral agents in persistent HIV pathogenesis.Retrovirology · 2018Review
- Kinetic Modeling of Virus Growth in Cells.Microbiology and molecular biology reviews : MMBR · 2018Review
- CRISPR-mediated Activation of Latent HIV-1 Expression.Molecular therapy : the journal of the American Society of Gene Therapy · 2016Article
- Review
- RNA interference approaches for treatment of HIV-1 infection.Genome medicine · 2015Article
- Silencing of HIV-1 gag gene from epidemic strains among men who have sex with men (MSM) in Tianjin, China by a broad-spectrum short hairpin RNA.Virusdisease · 2014Article
- Regulation of host gene expression by HIV-1 TAR microRNAs.Retrovirology · 2013Article
- siRNA Genome Screening Approaches to Therapeutic Drug Repositioning.Pharmaceuticals (Basel, Switzerland) · 2013Article
- Citrus tristeza virus: Evolution of Complex and Varied Genotypic Groups.Frontiers in microbiology · 2013Article
- Genetic selection for context-dependent stochastic phenotypes: Sp1 and TATA mutations increase phenotypic noise in HIV-1 gene expression.PLoS computational biology · 2013Article
- Creating genetic resistance to HIV.Current opinion in immunology · 2012Review
- Response to "HIV Escape From RNAi Antivirals: Yet Another Houdini Action?".Molecular therapy. Nucleic acids · 2012Article
- HIV-1 Escape From RNAi Antivirals: Yet Another Houdini Action?Molecular therapy. Nucleic acids · 2012Article
- HIV develops indirect cross-resistance to combinatorial RNAi targeting two distinct and spatially distant sites.Molecular therapy : the journal of the American Society of Gene Therapy · 2012Article
- Antiviral RNAi: translating science towards therapeutic success.Pharmaceutical research · 2011Review
- The HIV-1 Tat protein has a versatile role in activating viral transcription.Journal of virology · 2011Article
- An evolved adeno-associated viral variant enhances gene delivery and gene targeting in neural stem cells.Molecular therapy : the journal of the American Society of Gene Therapy · 2011Article
- Development of a low bias method for characterizing viral populations using next generation sequencing technology.PloS one · 2010Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
HIV can rapidly evolve when placed under selective pressure, including immune surveillance or the administration of antiretroviral drugs. Typically, a variant protein allows HIV to directly evade the selective pressure. Similarly, HIV has escaped suppression by RNA interference (RNAi) directed against viral RNAs by acquiring mutations at the target region that circumvent RNAi-mediated inhibition while conserving necessary viral functions. However, when we directed RNAi against the viral TAR hairpin, which plays an indispensable role in viral transcription, resistant strains were recovered, but none carried a mutation at the target site. Instead, we isolated several strains carrying promoter mutations that indirectly compensated for the RNAi by upregulating viral transcription. Combining RNAi with the application of an antiviral drug blocked replication of such mutants. Evolutionary tuning of viral transcriptional regulation may serve as a general evasion mechanism that may be targeted to improve the efficacy of antiviral therapy.
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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.