ReviewViruses2021
HIV-1: To Splice or Not to Splice, That Is the Question.
Review in Viruses, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
59 citing papers in PubMed, 71 citations in OpenAlex.
- HIV-1 Vif-dependent SUMOylation regulates viral RNA splicing.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Transcription start site heterogeneity controls MDA5 sensing of unspliced HIV-1 RNAs.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- A nanopore-based HIV-1 reference epitranscriptome.Nucleic acids research · 2026Article
- Article
- RNA splicing patterns contribute to burst size variation among HIV-1-infected Jurkat cell clones.Journal of virology · 2025Article
- Systematic identification and characterization of virus lncRNAs suggests extensive structural mimicry of host lncRNAs.Briefings in bioinformatics · 2025Article
- High-throughput screening and characterization of novel inhibitors targeting HIV-1 protease precursor autoprocessing.Scientific reports · 2025Article
- Comprehensive Transcriptome Annotation of Thousands of HIV-1 Genomes.bioRxiv : the preprint server for biology · 2025Article
- Lentiviral Vectors: From Wild-Type Viruses to Efficient Multi-Functional Delivery Vectors.International journal of molecular sciences · 2025Review
- 5' cap sequestration is required for sensing of unspliced HIV-1 RNA by MDA5.bioRxiv : the preprint server for biology · 2025Article
- MicroRNAs in HIV infection: dual regulators of viral replication and host immunity.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- HIV-1 Tat: Molecular Switch in Viral Persistence and Emerging Technologies for Functional Cure.International journal of molecular sciences · 2025Review
- Mapping HIV-1 RNA structure, homodimers, long-range interactions and persistent domains by HiCapR.eLife · 2025Article
- How to recover from a bad start: adaptation of HIV-1 transcription start site mutants during serial passaging in culture.Journal of virology · 2025Article
- Resolving sequencing-based HIV-1 epitranscriptomics.Epigenomics · 2025Review
- MrHAMER2: high-accuracy long-read RNA sequencing to decode isoform-specific variation in viral transcripts during latency.bioRxiv : the preprint server for biology · 2025Article
- The translational landscape of HIV-1 infected cells reveals key gene regulatory principles.Nature structural & molecular biology · 2025Article
- YTHDF1 and YTHDC1 mJournal of virology · 2025Article
- Article
- Mu opioid receptor activation in microglia enhances HIV-1 infection and HIV-infection-induced inflammatory responses.Frontiers in immunology · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The transcription of the HIV-1 provirus results in only one type of transcript-full length genomic RNA. To make the mRNA transcripts for the accessory proteins Tat and Rev, the genomic RNA must completely splice. The mRNA transcripts for Vif, Vpr, and Env must undergo splicing but not completely. Genomic RNA (which also functions as mRNA for the Gag and Gag/Pro/Pol precursor polyproteins) must not splice at all. HIV-1 can tolerate a surprising range in the relative abundance of individual transcript types, and a surprising amount of aberrant and even odd splicing; however, it must not over-splice, which results in the loss of full-length genomic RNA and has a dramatic fitness cost. Cells typically do not tolerate unspliced/incompletely spliced transcripts, so HIV-1 must circumvent this cell policing mechanism to allow some splicing while suppressing most. Splicing is controlled by RNA secondary structure, cis-acting regulatory sequences which bind splicing factors, and the viral protein Rev. There is still much work to be done to clarify the combinatorial effects of these splicing regulators. These control mechanisms represent attractive targets to induce over-splicing as an antiviral strategy. Finally, splicing has been implicated in latency, but to date there is little supporting evidence for such a mechanism. In this review we apply what is known of cellular splicing to understand splicing in HIV-1, and present data from our newer and more sensitive deep sequencing assays quantifying the different HIV-1 transcript types.
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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.