ArticleJournal of leukocyte biology2022
HIV-1-induced type I IFNs promote viral latency in macrophages.
Article in Journal of leukocyte biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 18 citations in OpenAlex.
- Tenofovir, Interferon Pathways, and Mucosal Immunity: Implications for People Living With HIV.American journal of reproductive immunology (New York, N.Y. : 1989) · 2026Review
- NF-κB-dependent and independent inflammatory responses during acute HIV-1 infection in a model of human microglia.Frontiers in immunology · 2026Article
- Cannabinoid Receptor Type 2 Agonist JWH-133 Stimulates Antiviral Factors and Decreases Proviral, Inflammatory, and Neurotoxic Proteins in HIV-Infected Macrophage Secretome.International journal of molecular sciences · 2025Article
- Article
- Cellular Tropism and Viral Genetics in Appendix Tissue Reservoirs of Subtype C HIV-1-Infected Aviremic Persons.The Journal of infectious diseases · 2025Article
- The Role of Type I Interferons in Tuberculosis and in Tuberculosis-Risk-Associated Comorbidities.Infectious disease reports · 2025Review
- Review
- The intestinal interferon system and specialized enterocytes as putative drivers of HIV latency.Frontiers in immunology · 2025Review
- HIV-induced RSAD2/Viperin supports sustained infection of monocyte-derived macrophages.Journal of virology · 2024Article
- Article
- Review
- A macrophage-cell model of HIV latency reveals the unusual importance of the bromodomain axis.Virology journal · 2024Article
- Dysregulated neuroimmune interactions and sustained type I interferon signaling after human immunodeficiency virus type 1 infection of human iPSC derived microglia and cerebral organoids.bioRxiv : the preprint server for biology · 2023Article
- Long Noncoding RNA Metastasis-Associated Lung Adenocarcinoma Transcript 1 Promotes HIV-1 Replication through Modulating microRNAs in Macrophages.Journal of virology · 2023Article
- Human cytomegalovirus UL138 interaction with USP1 activates STAT1 in infection.PLoS pathogens · 2023Article
- Human Cytomegalovirus UL138 Interaction with USP1 Activates STAT1 in infection.bioRxiv : the preprint server for biology · 2023Article
- SARS-CoV-2, HIV, and HPV: Convergent evolution of selective regulation of cGAS-STING signaling.Journal of medical virology · 2023Review
- HIV-1-induced type I IFNs promote viral latency in macrophages.Journal of leukocyte biology · 2022Article
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 1 institution in 1 country.
Funding
Abstract
Macrophages chronically infected with HIV-1 serve as a reservoir that contributes to HIV-1 persistence during antiretroviral therapy; however, the mechanisms governing the establishment and maintenance of this virus reservoir have not been fully elucidated. Here, we show that HIV-1 enters a state reminiscent of latency in monocyte-derived macrophages (MDMs), characterized by integrated proviral DNA with decreased viral transcription. This quiescent state is associated with decreased NF-κB p65, RNA polymerase II, and p-TEFb recruitment to the HIV-1 promoter as well as maintenance of promoter chromatin in a transcriptionally nonpermissive state. MDM transition to viral latency is mediated by type I IFN signaling, as inhibiting type I IFN signaling or blocking type 1 IFN prevents the establishment of latent infection. Knockdown studies demonstrate that the innate immune signaling molecule mitochondrial antiviral signaling protein (MAVS) is required for the transition to latency. Finally, we demonstrate a role for the viral accessory protein Vpr in the establishment of HIV-1 latency in macrophages. Our data indicate that HIV-1-induced type I IFN production is responsible for the establishment of viral latency in MDMs and identify possible therapeutic targets for the prevention or elimination of this important HIV-1 reservoir.
Indexed as
Identifiers
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.