ArticleJournal of virology1997
A naturally arising mutation of a potential silencer of exon splicing in human immunodeficiency virus type 1 induces dominant aberrant splicing and arrests virus production.
Article in Journal of virology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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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Who cites it
34 citing papers in PubMed, 56 citations in OpenAlex.
- Lentiviral Vectors: From Wild-Type Viruses to Efficient Multi-Functional Delivery Vectors.International journal of molecular sciences · 2025Review
- Review
- Dynamic nanopore long-read sequencing analysis of HIV-1 splicing events during the early steps of infection.Retrovirology · 2020Article
- Human Tat-specific factor 1 binds the HIV-1 genome and selectively transports HIV-1 RNAs.Molecular biology reports · 2020Article
- Focus on Translation Initiation of the HIV-1 mRNAs.International journal of molecular sciences · 2018Review
- Characterizing HIV-1 Splicing by Using Next-Generation Sequencing.Journal of virology · 2017Article
- Unusual Fusion Proteins of HIV-1.Frontiers in microbiology · 2016Review
- Article
- Natural single-nucleotide polymorphisms in the 3' region of the HIV-1 pol gene modulate viral replication ability.Journal of virology · 2014Article
- Identification of cis-acting elements and splicing factors involved in the regulation of BIM Pre-mRNA splicing.PloS one · 2014Article
- A syn-anti conformational difference allows SRSF2 to recognize guanines and cytosines equally well.The EMBO journal · 2012Article
- Article
- Role of cellular RNA processing factors in human immunodeficiency virus type 1 mRNA metabolism, replication, and infectivity.Journal of virology · 2009Article
- The secondary structure of the human immunodeficiency virus type 1 transcript modulates viral splicing and infectivity.Journal of virology · 2008Article
- Insights into the selective activation of alternatively used splice acceptors by the human immunodeficiency virus type-1 bidirectional splicing enhancer.Nucleic acids research · 2008Article
- Both linear and discontinuous ribosome scanning are used for translation initiation from bicistronic human immunodeficiency virus type 1 env mRNAs.Journal of virology · 2007Article
- The strength of the HIV-1 3' splice sites affects Rev function.Retrovirology · 2006Article
- Utilization of host SR protein kinases and RNA-splicing machinery during viral replication.Proceedings of the National Academy of Sciences of the United States of America · 2006Article
- The retrovirus RNA trafficking granule: from birth to maturity.Retrovirology · 2006Review
- Identification of splicing silencers and enhancers in sense Alus: a role for pseudoacceptors in splice site repression.Molecular and cellular biology · 2005Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
We have isolated a naturally arising human immunodeficiency type 1 (HIV-1) mutant containing a point mutation within the env gene. The point mutation resulted in complete loss of balanced splicing, with dominant production of aberrant mRNAs. The aberrant RNAs arose via activation of normally cryptic splice sites flanking the mutation within the env terminal exon to create exon 6D, which was subsequently incorporated in aberrant env, tat, rev, and nef mRNAs. Aberrant multiply spliced messages contributed to reduced virus replication as a result of a reduction in wild-type Rev protein. The point mutation within exon 6D activated exon 6D inclusion when the exon and its flanking splice sites were transferred to a heterologous minigene. Introduction of the point mutation into an otherwise wild-type HIV-1 proviral clone resulted in virus that was severely inhibited for replication in T cells and displayed elevated usage of exon 6D. Exon 6D contains a bipartite element similar to that seen in tat exon 3 of HIV-1, consisting of a potential exon splicing silencer (ESS) juxtaposed to a purine-rich sequence similar to known exon splicing enhancers. In the absence of a flanking 5' splice site, the point mutation within the exon 6D ESS-like element strongly activated env splicing, suggesting that the putative ESS plays a natural role in limiting the level of env splicing. We propose, therefore, that exon silencers may be a common element in the HIV-1 genome used to create balanced splicing of multiple products from a single precursor RNA.
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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.