ArticleJournal of virology2011
Single-nucleotide changes in the HIV Rev-response element mediate resistance to compounds that inhibit Rev function.
Article in Journal of virology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 25 citations in OpenAlex.
- Versatile HIV Rev-dependent reporter cell system for stringent and sensitive quantification of viral reservoirs, neutralizing antibodies, and restriction factors.Retrovirology · 2026Article
- Versatile HIV Rev-dependent reporter cell system for stringent and sensitive quantification of viral reservoirs, neutralizing antibodies, and restriction factors.bioRxiv : the preprint server for biology · 2025Article
- Article
- Rev-RRE activity modulates HIV-1 replication and latency reactivation: Implications for viral persistence and cure strategies.PLoS pathogens · 2025Article
- Suppression of viral rebound by a Rev-dependent lentiviral particle in SIV-infected rhesus macaques.Gene therapy · 2025Article
- Discovery of Ten Anti-HIV Hit Compounds and Preliminary Pharmacological Mechanisms StudiesCurrent HIV research · 2024Article
- HIV Preintegration Transcription and Host Antagonism.Current HIV research · 2023Article
- Limited nucleotide changes of HIV-1 subtype B Rev response element in China affect overall Rev-RRE activity and viral replication.Frontiers in microbiology · 2022Article
- Identification of an Antiretroviral Small Molecule That Appears To Be a Host-Targeting Inhibitor of HIV-1 Assembly.Journal of virology · 2021Article
- HIV Rev-isited.Open biology · 2020Review
- HIV-1 Rev interacts with HERV-K RcREs present in the human genome and promotes export of unspliced HERV-K proviral RNA.Retrovirology · 2019Article
- Review of Current Cell-Penetrating Antibody Developments for HIV-1 Therapy.Molecules (Basel, Switzerland) · 2018Review
- Discovery of Novel Small-Molecule Inhibitors of LIM Domain Kinase for Inhibiting HIV-1.Journal of virology · 2017Article
- Identification and Optimization of Thienopyridine Carboxamides as Inhibitors of HIV Regulatory Complexes.Antimicrobial agents and chemotherapy · 2017Article
- Rev-RRE Functional Activity Differs Substantially Among Primary HIV-1 Isolates.AIDS research and human retroviruses · 2016Article
- Characterization and in vitro activity of a branched peptide boronic acid that interacts with HIV-1 RRE RNA.Bioorganic & medicinal chemistry · 2016Article
- Importance of codon usage for the temporal regulation of viral gene expression.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Functional analyses reveal extensive RRE plasticity in primary HIV-1 sequences selected under selective pressure.PloS one · 2014Article
- Limited nucleotide changes in the Rev response element (RRE) during HIV-1 infection alter overall Rev-RRE activity and Rev multimerization.Journal of virology · 2013Article
- Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Previously we described the identification of two compounds (3-amino-5-ethyl-4,6-dimethylthieno[2,3-b]pyridine-2-carboxamide [103833] and 4-amino-6-methoxy-2-(trifluoromethyl)-3-quinolinecarbonitrile [104366]) that interfered with HIV replication through the inhibition of Rev function. We now describe resistant viral variants that arose after drug selection, using virus derived from two different HIV proviral clones, NL4-3 and R7/3. With HIV(NL4-3), each compound selected a different single point mutation in the Rev response element (RRE) at the bottom of stem-loop IIC. Either mutation led to the lengthening of the stem-loop IIC stem by an additional base pair, creating an RRE that was more responsive to lower concentrations of Rev than the wild type. Surprisingly, wild-type HIV(R7/3) was also found to be inhibited when tested with these compounds, in spite of the fact this virus already has an RNA stem-loop IIC similar to the one in the resistant NL4-3 variant. When drug resistance was selected in HIV(R7/3), a virus arose with two nucleotide changes that mapped to the envelope region outside the RRE. One of these nucleotide changes was synonymous with respect to env, and one was not. The combination of both nucleotide changes appeared to be necessary for the resistance phenotype as the individual point mutations by themselves did not convey resistance. Thus, although drug-resistant variants can be generated with both viral strains, the underlying mechanism is clearly different. These results highlight that minor nucleotide changes in HIV RNA, outside the primary Rev binding site, can significantly alter the efficiency of the Rev/RRE pathway.
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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.