ArticlemBio2020
Reversal of Epigenetic Silencing Allows Robust HIV-1 Replication in the Absence of Integrase Function.
Article in mBio, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
23 citing papers in PubMed, 26 citations in OpenAlex.
- A Leap Forward in Vaccination - the Epigenetic Silencing of HIV by cVacc.Current HIV/AIDS reports · 2026Review
- Non-integrase mechanisms for dolutegravir resistance.Retrovirology · 2026Review
- Epigenetic drugs against human DNA viruses and retroviruses.Antiviral research · 2025Review
- Expression of HIV from a 1-LTR circular DNA in the absence of integration.Retrovirology · 2025Article
- Brief Histories of Retroviral Integration Research and Associated International Conferences.Viruses · 2024Review
- Epistatic pathways can drive HIV-1 escape from integrase strand transfer inhibitors.Science advances · 2024Article
- Capsid-host interactions for HIV-1 ingress.Microbiology and molecular biology reviews : MMBR · 2023Review
- HIV-1 3'-Polypurine Tract Mutations Confer Dolutegravir Resistance by Switching to an Integration-Independent Replication Mechanism via 1-LTR Circles.Journal of virology · 2023Article
- The SMC5/6 complex: An emerging antiviral restriction factor that can silence episomal DNA.PLoS pathogens · 2023Article
- HIV Preintegration Transcription and Host Antagonism.Current HIV research · 2023Article
- Epigenetic silencing by the SMC5/6 complex mediates HIV-1 latency.Nature microbiology · 2022Article
- Mutations in the 3'-PPT Lead to HIV-1 Replication without Integration.Journal of virology · 2022Article
- Two lymphoid cell lines potently silence unintegrated HIV-1 DNAs.Retrovirology · 2022Article
- Multimodal Functionalities of HIV-1 Integrase.Viruses · 2022Review
- CHAF1A/B mediate silencing of unintegrated HIV-1 DNAs early in infection.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Mutations in the HIV-1 3'-Polypurine Tract Can Confer Dolutegravir Resistance.Antimicrobial agents and chemotherapy · 2022Article
- Silencing of Unintegrated Retroviral DNAs.Viruses · 2021Review
- Tax Induces the Recruitment of NF-κB to Unintegrated HIV-1 DNA To Rescue Viral Gene Expression and Replication.Journal of virology · 2021Article
- Long-Acting Cabotegravir for HIV/AIDS Prophylaxis.Biochemistry · 2021Review
- Elucidating the Basis for Permissivity of the MT-4 T-Cell Line to Replication of an HIV-1 Mutant Lacking the gp41 Cytoplasmic Tail.Journal of virology · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Integration of the proviral DNA intermediate into the host cell genome normally represents an essential step in the retroviral life cycle. While the reason(s) for this requirement remains unclear, it is known that unintegrated proviral DNA is epigenetically silenced. Here, we demonstrate that human immunodeficiency virus 1 (HIV-1) mutants lacking a functional integrase (IN) can mount a robust, spreading infection in cells expressing the Tax transcription factor encoded by human T-cell leukemia virus 1 (HTLV-1). In these cells, HIV-1 forms episomal DNA circles, analogous to hepatitis B virus (HBV) covalently closed circular DNAs (cccDNAs), that are transcriptionally active and fully capable of supporting viral replication. In the presence of Tax, induced NF-κB proteins are recruited to the long terminal repeat (LTR) promoters present on unintegrated HIV-1 DNA, and this recruitment in turn correlates with the loss of inhibitory epigenetic marks and the acquisition of activating marks on histones bound to viral DNA. Therefore, HIV-1 is capable of replication in the absence of integrase function if the epigenetic silencing of unintegrated viral DNA can be prevented or reversed.
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What OpenQuestion holds
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.