ArticleVirology2011
HIV latency is influenced by regions of the viral genome outside of the long terminal repeats and regulatory genes.
Article in Virology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed.
- Extensive proteomic and transcriptomic changes quench the TCR/CD3 activation signal of latently HIV-1 infected T cells.PLoS pathogens · 2021Article
- HIV-1 Latency and Latency Reversal: Does Subtype Matter?Viruses · 2019Review
- HIV Silencing and Inducibility Are Heterogeneous and Are Affected by Factors Intrinsic to the Virus.mBio · 2019Article
- Dynamics of HIV latency and reactivation in a primary CD4+ T cell model.PLoS pathogens · 2014Article
- Mechanisms of HIV Transcriptional Regulation and Their Contribution to Latency.Molecular biology international · 2012Article
- Facts and fiction: cellular models for high throughput screening for HIV-1 reactivating drugs.Current HIV research · 2011Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
We have previously described an in vitro primary thymocyte model for HIV latency that recapitulates several important aspects of latently infected cells obtained from patients. Our original model included a truncated HIV genome expressing only Tat, Rev, and Vpu along with a reporter gene. We have now expanded these studies to include reporter viruses encoding more complete viral genomes. We show here that regions of the viral genome outside of the long terminal repeat promoter and Tat/Rev regulatory genes can substantially affect both the basal level of HIV transcription prior to stimulation, and also the level of viral expression following costimulation via CD3 and CD28 ligation. These differences in latency phenotype between truncated and more complete HIV genomes demonstrate the importance of accessory genes in the context of HIV latency and indicate that care should be taken when interpreting data derived from heavily modified HIV genomes in latency models.
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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.