ReviewViruses2013
Viral and cellular requirements for the nuclear entry of retroviral preintegration nucleoprotein complexes.
Review in Viruses, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
81 citing papers in PubMed.
- Mis-localized nucleoporin POM121C potently inhibits nuclear entry of HIV-1 but leads to the outgrowth of viral escape mutants.Journal of virology · 2026Article
- HIV-1 capsid interactions with Nuclear Pore Complex components support nuclear entry via affinity gradient.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Reprogramming innate immunity through viral interference: A double-edged strategy for enhancing and containing gene therapies.Molecular therapy. Nucleic acids · 2026Review
- Direct visualization of HIV-1 core nuclear import and its interplay with the nuclear pore.EMBO reports · 2025Article
- Translocation of HIV capsid core through the Nuclear Pore Complex by affinity gradient.bioRxiv : the preprint server for biology · 2025Article
- Impact of HIV-1 capsid polymorphisms on viral infectivity and susceptibility to lenacapavir.mBio · 2025Article
- Three Prime Repair Exonuclease 1 preferentially degrades the integration-incompetent HIV-1 DNA through favorable kinetics, thermodynamic, structural and conformational properties.bioRxiv : the preprint server for biology · 2024Article
- HIV-1 capsid and viral DNA integration.mBio · 2024Review
- Murine leukemia virus infection of non-dividing dendritic cells is dependent on nucleoporins.PLoS pathogens · 2024Article
- The HIV-1 capsid core is an opportunistic nuclear import receptor.Nature communications · 2023Article
- RANBP2 and USP9x regulate nuclear import of adenovirus minor coat protein IIIa.PLoS pathogens · 2022Article
- Repair of APOBEC3G-Mutated Retroviral DNAJournal of virology · 2021Article
- Human Three Prime Repair Exonuclease 1 Promotes HIV-1 Integration by Preferentially Degrading Unprocessed Viral DNA.Journal of virology · 2021Article
- HIV-1 uncoating occurs via a series of rapid biomechanical changes in the core related to individual stages of reverse transcription.Journal of virology · 2021Article
- Measuring the subcellular compartmentalization of viral infections by protein complementation assay.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- HIV-1 Hijacking of Host ATPases and GTPases That Control Protein Trafficking.Frontiers in cell and developmental biology · 2021Review
- Strategies for Targeting Retroviral Integration for Safer Gene Therapy: Advances and Challenges.Frontiers in molecular biosciences · 2021Review
- Transportin-1: A Nuclear Import Receptor with Moonlighting Functions.Frontiers in molecular biosciences · 2021Review
- Capsid Lattice Destabilization Leads to Premature Loss of the Viral Genome and Integrase Enzyme during HIV-1 Infection.Journal of virology · 2020Article
- HIV-1 resists MxB inhibition of viral Rev protein.Emerging microbes & infections · 2020Article
21 more citing papers are in PubMed but not listed here.
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.
Funding
Abstract
Retroviruses integrate their reverse transcribed genomes into host cell chromosomes as an obligate step in virus replication. The nuclear envelope separates the chromosomes from the cell cytoplasm during interphase, and different retroviral groups deal with this physical barrier in different ways. Gammaretroviruses are dependent on the passage of target cells through mitosis, where they are believed to access chromosomes when the nuclear envelope dissolves for cell division. Contrastingly, lentiviruses such as HIV-1 infect non-dividing cells, and are believed to enter the nucleus by passing through the nuclear pore complex. While numerous virally encoded elements have been proposed to be involved in HIV-1 nuclear import, recent evidence has highlighted the importance of HIV-1 capsid. Furthermore, capsid was found to be responsible for the viral requirement of various nuclear transport proteins, including transportin 3 and nucleoporins NUP153 and NUP358, during infection. In this review, we describe our current understanding of retroviral nuclear import, with emphasis on recent developments on the role of the HIV-1 capsid protein.
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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.