ArticleJournal of virology2013
An intronic G run within HIV-1 intron 2 is critical for splicing regulation of vif mRNA.
Article in Journal of virology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 37 citations in OpenAlex.
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- SRSF1 acts as an IFN-I-regulated cellular dependency factor decisively affecting HIV-1 post-integration steps.Frontiers in immunology · 2022Article
- Altered HIV-1 mRNA Splicing Due to Drug-Resistance-Associated Mutations in Exon 2/2b.International journal of molecular sciences · 2021Article
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- HIV-1: To Splice or Not to Splice, That Is the Question.Viruses · 2021Review
- Dynamic nanopore long-read sequencing analysis of HIV-1 splicing events during the early steps of infection.Retrovirology · 2020Article
- A scale-free analysis of the HIV-1 genome demonstrates multiple conserved regions of structural and functional importance.PLoS computational biology · 2019Article
- Gymnotic Delivery of LNA Mixmers Targeting Viral SREs Induces HIV-1 mRNA Degradation.International journal of molecular sciences · 2019Article
- Expression Level of HIV-1 Vif Can Be Fluctuated by Natural Nucleotide Variations in theFrontiers in microbiology · 2019Article
- Global synonymous mutagenesis identifies cis-acting RNA elements that regulate HIV-1 splicing and replication.PLoS pathogens · 2018Article
- Elucidating the in vivo interactome of HIV-1 RNA by hybridization capture and mass spectrometry.Scientific reports · 2017Article
- Analysis of Competing HIV-1 Splice Donor Sites Uncovers a Tight Cluster of Splicing Regulatory Elements within Exon 2/2b.Journal of virology · 2017Article
- Identification of small molecule modulators of HIV-1 Tat and Rev protein accumulation.Retrovirology · 2017Article
- Production of HIV-1Frontiers in microbiology · 2017Article
- Natural Single-Nucleotide Variations in the HIV-1 Genomic SA1prox Region Can Alter Viral Replication Ability by Regulating Vif Expression Levels.Journal of virology · 2016Article
- Balanced splicing at the Tat-specific HIV-1 3'ss A3 is critical for HIV-1 replication.Retrovirology · 2015Article
- Biophysical Characterization of Nucleophosmin Interactions with Human Immunodeficiency Virus Rev and Herpes Simplex Virus US11.PloS one · 2015Article
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Authors and funding
15 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Within target T lymphocytes, human immunodeficiency virus type I (HIV-1) encounters the retroviral restriction factor APOBEC3G (apolipoprotein B mRNA-editing enzyme, catalytic polypeptide-like 3G; A3G), which is counteracted by the HIV-1 accessory protein Vif. Vif is encoded by intron-containing viral RNAs that are generated by splicing at 3' splice site (3'ss) A1 but lack splicing at 5'ss D2, which results in the retention of a large downstream intron. Hence, the extents of activation of 3'ss A1 and repression of D2, respectively, determine the levels of vif mRNA and thus the ability to evade A3G-mediated antiviral effects. The use of 3'ss A1 can be enhanced or repressed by splicing regulatory elements that control the recognition of downstream 5'ss D2. Here we show that an intronic G run (G(I2)-1) represses the use of a second 5'ss, termed D2b, that is embedded within intron 2 and, as determined by RNA deep-sequencing analysis, is normally inefficiently used. Mutations of G(I2)-1 and activation of D2b led to the generation of transcripts coding for Gp41 and Rev protein isoforms but primarily led to considerable upregulation of vif mRNA expression. We further demonstrate, however, that higher levels of Vif protein are actually detrimental to viral replication in A3G-expressing T cell lines but not in A3G-deficient cells. These observations suggest that an appropriate ratio of Vif-to-A3G protein levels is required for optimal virus replication and that part of Vif level regulation is effected by the novel G run identified here.
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