ArticlePLoS pathogens2013
24 hours in the life of HIV-1 in a T cell line.
Article in PLoS pathogens, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 92 papers, 2 of them syntheses that pooled it.
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
92 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Genetic variation near CXCL12 is associated with susceptibility to HIV-related non-Hodgkin lymphoma.Haematologica · 2021Pooled it
- Identification and characterization of a long non-coding RNA up-regulated during HIV-1 infection.Virology · 2017Pooled it
- The Activation State of CD4 T Cells Alters Cellular Peptidase Activities, HIV Antigen Processing, and MHC Class I Presentation in a Sequence-Dependent Manner.Journal of immunology (Baltimore, Md. : 1950) · 2019Trial
- Blocking Host Factors IAP and DDX3 Activates HIV-1 Transcription and Increases Apoptosis Sensitivity of HIV-1 Infected Cells.Pathogens (Basel, Switzerland) · 2026Article
- Effect of TAR hairpin stabilization on HIV-1 reverse transcription.Journal of virology · 2026Article
- Transcriptomic Profiling Identifies TALAM1 and LINC00702 as HIV-1-Responsive lncRNAs in Microglia.International journal of molecular sciences · 2026Article
- Substantial deceleration of adaptation of HIV-1 within 1500 generations in an experimental evolution: a genomic perspective.Virus evolution · 2026Article
- The HIV-1 Vpr R77Q mutant alters host apoptotic gene regulation in CD4+ T cells.Frontiers in cellular and infection microbiology · 2026Article
- The immunosuppressive tuberculosis-associated microenvironment inhibits viral replication and promotes HIV-1 latency in CD4iScience · 2024Article
- HIHISIV: a database of gene expression in HIV and SIV host immune response.BMC bioinformatics · 2024Article
- HIV-1 Gag co-localizes with euchromatin histone marks at the nuclear periphery.Journal of virology · 2023Article
- POLE3 is a repressor of unintegrated HIV-1 DNA required for efficient virus integration and escape from innate immune sensing.Science advances · 2023Article
- CD8Nature communications · 2023Article
- Single-Cell Transcriptomics ofCells · 2023Review
- Article
- HIV-1 virological synapse formation enhances infection spread by dysregulating Aurora Kinase B.PLoS pathogens · 2023Article
- Article
- The Persistence of HIV Diversity, Transcription, and Nef Protein in Kaposi's Sarcoma Tumors during Antiretroviral Therapy.Viruses · 2022Article
- The HIV-1 proviral landscape reveals that Nef contributes to HIV-1 persistence in effector memory CD4+ T cells.The Journal of clinical investigation · 2022Article
- Study on Pharmacokinetic Interactions Between HS-10234 and Emtricitabine in Healthy Subjects: An Open-Label, Two-Sequence, Self-Controlled Phase I Trial.Infectious diseases and therapy · 2022Article
32 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
HIV-1 infects CD4+ T cells and completes its replication cycle in approximately 24 hours. We employed repeated measurements in a standardized cell system and rigorous mathematical modeling to characterize the emergence of the viral replication intermediates and their impact on the cellular transcriptional response with high temporal resolution. We observed 7,991 (73%) of the 10,958 expressed genes to be modulated in concordance with key steps of viral replication. Fifty-two percent of the overall variability in the host transcriptome was explained by linear regression on the viral life cycle. This profound perturbation of cellular physiology was investigated in the light of several regulatory mechanisms, including transcription factors, miRNAs, host-pathogen interaction, and proviral integration. Key features were validated in primary CD4+ T cells, and with viral constructs using alternative entry strategies. We propose a model of early massive cellular shutdown and progressive upregulation of the cellular machinery to complete the viral life cycle.
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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.