ArticleVirology2010
An altered and more efficient mechanism of CCR5 engagement contributes to macrophage tropism of CCR5-using HIV-1 envelopes.
Article in Virology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 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.
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Who cites it
39 citing papers in PubMed, 61 citations in OpenAlex.
- Review
- Glycan dependent phenotype differences of HIV-1 generated from macrophage versus CD4Frontiers in immunology · 2023Article
- HIV-1 cell-to-cell spread overcomes the virus entry block of non-macrophage-tropic strains in macrophages.PLoS pathogens · 2022Article
- Modular Lentiviral Vectors for Highly Efficient Transgene Expression in Resting Immune Cells.Viruses · 2021Article
- Longitudinal analysis of subtype C envelope tropism for memory CD4Retrovirology · 2020Article
- CXCR4-Using HIV Strains Predominate in Naive and Central Memory CD4Journal of virology · 2020Article
- No detection of CD4-independent human immunodeficiency virus 1 envelope glycoproteins in brain tissue of patients with or without neurological complications.Archives of virology · 2019Article
- CCR5 structural plasticity shapes HIV-1 phenotypic properties.PLoS pathogens · 2018Article
- Molecular Signatures of HIV-1 Envelope Associated with HIV-Associated Neurocognitive Disorders.Current HIV/AIDS reports · 2018Review
- Article
- Delineating CD4 dependency of HIV-1: Adaptation to infect low level CD4 expressing target cells widens cellular tropism but severely impacts on envelope functionality.PLoS pathogens · 2017Article
- Frequency and Env determinants of HIV-1 subtype C strains from antiretroviral therapy-naive subjects that display incomplete inhibition by maraviroc.Retrovirology · 2016Article
- Toxicity and in vitro activity of HIV-1 latency-reversing agents in primary CNS cells.Journal of neurovirology · 2016Article
- Reduced Baseline Sensitivity to Maraviroc Inhibition Among R5 HIV-1 Isolates From Individuals With Severe Immunodeficiency.Journal of acquired immune deficiency syndromes (1999) · 2016Article
- CCR5 susceptibility to ligand-mediated down-modulation differs between human T lymphocytes and myeloid cells.Journal of leukocyte biology · 2015Article
- Article
- Periluminal Distribution of HIV-Binding Target Cells and Gp340 in the Oral, Cervical and Sigmoid/Rectal Mucosae: A Mapping Study.PloS one · 2015Article
- Single genome analysis reveals genetic characteristics of Neuroadaptation across HIV-1 envelope.Retrovirology · 2014Article
- T cells detect intracellular DNA but fail to induce type I IFN responses: implications for restriction of HIV replication.PloS one · 2014Article
- HIV-1 envelope-receptor interactions required for macrophage infection and implications for current HIV-1 cure strategies.Journal of leukocyte biology · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 5 institutions in 2 countries.
Funding
Abstract
While CCR5 is the principal coreceptor used by macrophage (M)-tropic HIV-1, not all primary CCR5-using (R5) viruses enter macrophages efficiently. Here, we used functionally-diverse R5 envelope (Env) clones to characterize virus-cell interactions important for efficient CCR5-mediated macrophage entry. The magnitude of macrophage entry by Env-pseudotyped reporter viruses correlated with increased immunoreactivity of CD4-induced gp120 epitopes, increased ability to scavenge low levels of cell-surface CCR5, reduced sensitivity to the CCR5 inhibitor maraviroc, and increased dependence on specific residues in the CCR5 ECL2 region. These results are consistent with an altered and more efficient mechanism of CCR5 engagement. Structural studies revealed potential alterations within the gp120 V3 loop, the gp41 interaction sites at the gp120 C- and N-termini, and within the gp120 CD4 binding site which may directly or indirectly lead to more efficient CCR5-usage. Thus, enhanced gp120-CCR5 interactions may contribute to M-tropism of R5 HIV-1 strains through different structural mechanisms.
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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.