ArticleJournal of virology2013
A doubly fluorescent HIV-1 reporter shows that the majority of integrated HIV-1 is latent shortly after infection.
Article in Journal of virology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 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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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.
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Who cites it
77 citing papers in PubMed, 110 citations in OpenAlex.
- Three immunoregulatory signatures define non-productive HIV infection in stem cell memory CD4Nature communications · 2026Article
- HIV-1 establishes immediate latency in T cells expressing the viral Nef protein.FEBS open bio · 2026Article
- Three immunoregulatory signatures define non-productive HIV infection in CD4bioRxiv : the preprint server for biology · 2026Article
- Investigating the dynamics of proviral silencing in polyclonal HIV-1 infected Jurkat cell populations.bioRxiv : the preprint server for biology · 2026Article
- Article
- Limitations and use of the Morpheus-V5 dual reporter virus in assessing interventions that target HIV latency.Journal of virological methods · 2025Article
- Development and characterization of a double-fluorescent HIV-1 reporter cellular model to tackle the Rev-dependent export pathway.Microbiology spectrum · 2025Article
- Reporter-expressing viruses for antiviral drug discovery research.Frontiers in cellular and infection microbiology · 2025Review
- The Proviral Reservoirs of Human Immunodeficiency Virus (HIV) Infection.Pathogens (Basel, Switzerland) · 2024Review
- CBP/p300 lysine acetyltransferases inhibit HIV-1 expression in latently infected T cells.iScience · 2024Article
- Variation in HIV-1 Tat activity is a key determinant in the establishment of latent infection.JCI insight · 2024Article
- Mitotic deacetylase complex (MiDAC) recognizes the HIV-1 core promoter to control activated viral gene expression.PLoS pathogens · 2024Article
- HIV-Tocky system to visualize proviral expression dynamics.Communications biology · 2024Article
- Small molecule inhibitors of transcriptional cyclin-dependent kinases impose HIV-1 latency, presenting "block and lock" treatment strategies.Antimicrobial agents and chemotherapy · 2024Article
- A Canadian Survey of Research on HIV-1 Latency-Where Are We Now and Where Are We Heading?Viruses · 2024Review
- Experimental models for HIV latency and molecular tools for reservoir quantification-an update.Clinical microbiology reviews · 2023Review
- CDK8 inhibitors antagonize HIV-1 reactivation and promote provirus latency in T cells.Journal of virology · 2023Article
- Upstream Stimulatory Factors Regulate HIV-1 Latency and Are Required for Robust T Cell Activation.Viruses · 2023Article
- Inhibition of the TRIM24 bromodomain reactivates latent HIV-1.Scientific reports · 2023Article
- Epigenetic silencing by the SMC5/6 complex mediates HIV-1 latency.Nature microbiology · 2022Article
17 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
4 authors at 2 institutions in 2 countries.
Funding
Abstract
HIV-1 latency poses a major barrier to viral eradication. Canonically, latency is thought to arise from progressive epigenetic silencing of active infections. However, little is known about when and how long terminal repeat (LTR)-silent infections arise since the majority of the current latency models cannot differentiate between initial (LTR-silent) and secondary (progressive silencing) latency. In this study, we constructed and characterized a novel, double-labeled HIV-1 vector (Red-Green-HIV-1 [RGH]) that allows for detection of infected cells independently of LTR activity. Infection of Jurkat T cells and other cell lines with RGH suggests that the majority of integrated proviruses were LTR-silent early postinfection. Furthermore, the LTR-silent infections were transcriptionally competent, as the proviruses could be reactivated by a variety of T cell signaling agonists. Moreover, we used the double-labeled vector system to compare LTRs from seven different subtypes with respect to LTR silencing and reactivation. These experiments indicated that subtype D and F LTRs were more sensitive to silencing, whereas the subtype AE LTR was largely insensitive. Lastly, infection of activated human primary CD4(+) T cells yielded LTR-silent as well as productive infections. Taken together, our data, generated using the newly developed RGH vector as a sensitive tool to analyze HIV-1 latency on a single-cell level, show that the majority of HIV-1 infections are latent early postinfection.
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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.