ReviewViruses2011
Viral determinants of HIV-1 macrophage tropism.
Review in Viruses, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 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
47 citing papers in PubMed, 72 citations in OpenAlex.
- Comprehensive mapping of the virus and host factors that guide the paths of HIV-1 escape from a therapeutic.Cell reports · 2026Article
- Nanobody-Based Bioconjugates as Potent and Broadly Active Inhibitors of HIV Entry.Journal of the American Chemical Society · 2026Article
- EZ-DMS - A Simple and Accessible Protocol and Software Package for Deep Mutational Scanning of Virus Proteins.bioRxiv : the preprint server for biology · 2026Article
- Comprehensive Mapping of the Virus and Host Factors that Guide the Paths of HIV-1 Escape from a Therapeutic.bioRxiv : the preprint server for biology · 2025Article
- Prediction of the Co-receptor usage of the main worldwide HIV-1 subtypes, CRF, and CRF35-AD in Iranian patients via the five genotypic tools.Biochemistry and biophysics reports · 2025Article
- Rapid systemic spread and minimal immune responses following SIVsab intrarectal transmission in African green monkeys.JCI insight · 2024Article
- New Therapies and Strategies to Curb HIV Infections with a Focus on Macrophages and Reservoirs.Viruses · 2024Review
- HIV-1 Myeloid Reservoirs - Contributors to Viral Persistence and Pathogenesis.Current HIV/AIDS reports · 2024Review
- Fentanyl dysregulates neuroinflammation and disrupts blood-brain barrier integrity in HIV-1 Tat transgenic mice.Journal of neurovirology · 2024Article
- Antigen Presenting Cell-Mediated HIV-1Medical research archives · 2023Article
- HIV Latency in Myeloid Cells: Challenges for a Cure.Pathogens (Basel, Switzerland) · 2022Review
- HIV-1 cell-to-cell spread overcomes the virus entry block of non-macrophage-tropic strains in macrophages.PLoS pathogens · 2022Article
- The Roles of Amphibian (Viruses · 2021Article
- The Landscape of IFN/ISG Signaling in HIV-1-Infected Macrophages and Its Possible Role in the HIV-1 Latency.Cells · 2021Review
- TLR5-Mediated Reactivation of Quiescent Ranavirus FV3 inJournal of virology · 2021Article
- Article
- Review
- Current and Future Therapeutic Strategies for Lentiviral Eradication from Macrophage Reservoirs.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2019Review
- Synthesis and characterization of a long-acting emtricitabine prodrug nanoformulation.International journal of nanomedicine · 2019Article
- CCR5 structural plasticity shapes HIV-1 phenotypic properties.PLoS pathogens · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Macrophages are important target cells for HIV-1 infection that play significant roles in the maintenance of viral reservoirs and other aspects of pathogenesis. Understanding the determinants of HIV-1 tropism for macrophages will inform HIV-1 control and eradication strategies. Tropism for macrophages is both qualitative (infection or not) and quantitative (replication capacity). For example many R5 HIV-1 isolates cannot infect macrophages, but for those that can the macrophage replication capacity can vary by up to 1000-fold. Some X4 viruses are also capable of replication in macrophages, indicating that cellular tropism is partially independent of co-receptor preference. Preliminary data obtained with a small number of transmitted/founder viruses indicate inefficient macrophage infection, whereas isolates from later in disease are more frequently tropic for macrophages. Thus tropism may evolve over time, and more macrophage tropic viruses may be implicated in the pathogenesis of advanced HIV-1 infection. Compartmentalization of macrophage-tropic brain-derived envelope glycoproteins (Envs), and non-macrophage tropic non-neural tissue-derived Envs points to adaptation of HIV-1 quasi-species in distinct tissue microenvironments. Mutations within and adjacent to the Env-CD4 binding site have been identified that determine macrophage tropism at the entry level, but post-entry molecular determinants of macrophage replication capacity involving HIV-1 accessory proteins need further definition.
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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.