ReviewViruses2014
HIV-1 latency in monocytes/macrophages.
Review in Viruses, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 135 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
135 citing papers in PubMed.
- Implications of HIV persistence and pathogenesis in microglia.Current opinion in HIV and AIDS · 2026Review
- The Rectal Mucosal Myeloid Niche in HIV-1 Persistence: Reservoir Support, Viral Sequestration, and Therapeutic Opportunities.Viruses · 2026Review
- Latent HIV Reservoirs in the Central Nervous System: Mechanisms, Barriers, and Therapeutic Approaches.ACS infectious diseases · 2026Review
- Mitogen-Activated Protein Kinases: Therapeutic Signaling Catalysts in Viral Immune Evasion.Pathogens (Basel, Switzerland) · 2026Review
- Epigenetic mechanisms of retroviral regulation: a comparative review.Epigenetics & chromatin · 2026Review
- Modulation of IRF7-driven transcription as a strategy to control HIV-1 latency.Frontiers in immunology · 2026Article
- LncRNA TLR8-AS1 Restricts HIV-1 Infection and Inflammation in Macrophages by Suppressing Arachidonic Acid Metabolism Through NFAT1.Journal of inflammation research · 2026Article
- Age-Associated Expansion of HIV/SIV Reservoirs in People With HIV and SIV-Infected Macaques.Aging cell · 2025Article
- Kaposi's Sarcoma: A Non-Communicable Outcome Mainly Prompted by Communicable Diseases in Sub-Saharan Africa.International journal of molecular sciences · 2025Review
- Immuno-cell metabolic changes in HIV-1 infection.Infectious diseases & immunity · 2025Review
- Macrophage-Derived Factors with the Potential to Contribute to the Pathogenicity of HIV-1 and HIV-2: Roles of M-CSF and CXCL7.International journal of molecular sciences · 2025Article
- Yoda1, a Piezo1 agonist, induced latent HIV reactivation associated with upregulation of CD3/TCR complex and HLA genes.Research square · 2025Article
- Host factor Naf1 restricts HIV-1 infection of myeloid cells and compromises the capacity of dendritic cell to prime CD4Virologica Sinica · 2025Article
- Effect of Kinases in Extracellular Vesicles from HIV-1-Infected Cells on Bystander Cells.Cells · 2025Article
- The HIV-1 Transcriptional Program: From Initiation to Elongation Control.Journal of molecular biology · 2025Review
- Interleukin-32: a Pandora's box in human immunodeficiency virus infection.Frontiers in immunology · 2025Review
- Interaction of chikungunya virus glycoproteins with macrophage factors controls virion production.The EMBO journal · 2024Article
- Gesicles packaging dCas9-VPR ribonucleoprotein complexes can combine with vorinostat and promote HIV proviral transcription.Molecular therapy. Methods & clinical development · 2024Article
- Cognitive Impairment in People Living with HIV and the Impact of Mood: Results from a Cross-Sectional Study.Journal of clinical medicine · 2024Article
- Optimal therapy for HIV infection containment and virions inhibition.Infectious Disease Modelling · 2024Article
75 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
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human immunodeficiency virus type 1 (HIV-1) targets CD4+ T cells and cells of the monocyte/macrophage lineage. HIV pathogenesis is characterized by the depletion of T lymphocytes and by the presence of a population of cells in which latency has been established called the HIV-1 reservoir. Highly active antiretroviral therapy (HAART) has significantly improved the life of HIV-1 infected patients. However, complete eradication of HIV-1 from infected individuals is not possible without targeting latent sources of infection. HIV-1 establishes latent infection in resting CD4+ T cells and findings indicate that latency can also be established in the cells of monocyte/macrophage lineage. Monocyte/macrophage lineage includes among others, monocytes, macrophages and brain resident macrophages. These cells are relatively more resistant to apoptosis induced by HIV-1, thus are important stable hideouts of the virus. Much effort has been made in the direction of eliminating HIV-1 resting CD4+ T-cell reservoirs. However, it is impossible to achieve a cure for HIV-1 without considering these neglected latent reservoirs, the cells of monocyte/macrophage lineage. In this review we will describe our current understanding of the mechanism of latency in monocyte/macrophage lineage and how such cells can be specifically eliminated from the infected host.
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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 Socratic graph.