ArticleJournal of virology1999
Expanded tropism of primary human immunodeficiency virus type 1 R5 strains to CD4(+) T-cell lines determined by the capacity to exploit low concentrations of CCR5.
Article in Journal of virology, 1999. 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, 49 citations in OpenAlex.
- TILRR Promotes Migration of Immune Cells Through Induction of Soluble Inflammatory Mediators.Frontiers in cell and developmental biology · 2020Article
- V1 and V2 Domains of HIV Envelope Contribute to CCR5 Antagonist Resistance.Journal of virology · 2019Article
- 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
- Distinct HIV-1 entry phenotypes are associated with transmission, subtype specificity, and resistance to broadly neutralizing antibodies.Retrovirology · 2014Article
- Bioinformatic analysis of HIV-1 entry and pathogenesis.Current HIV research · 2014Review
- Affinofile profiling: how efficiency of CD4/CCR5 usage impacts the biological and pathogenic phenotype of HIV.Virology · 2013Review
- Generation of transmitted/founder HIV-1 infectious molecular clones and characterization of their replication capacity in CD4 T lymphocytes and monocyte-derived macrophages.Journal of virology · 2012Article
- Multiple CCR5 conformations on the cell surface are used differentially by human immunodeficiency viruses resistant or sensitive to CCR5 inhibitors.Journal of virology · 2011Article
- Variation in the biological properties of HIV-1 R5 envelopes: implications of envelope structure, transmission and pathogenesis.Future virology · 2010Article
- [CCR5 antagonists and HIV-1 infection: Bases and consequences of this therapeutic approach].Antibiotiques (Paris, France : 1999) · 2010Article
- Effective activation alleviates the replication block of CCR5-tropic HIV-1 in chimpanzee CD4+ lymphocytes.Virology · 2009Article
- An alteration of human immunodeficiency virus gp41 leads to reduced CCR5 dependence and CD4 independence.Journal of virology · 2008Article
- Exceptional molecular and coreceptor-requirement properties of molecular clones isolated from an Human Immunodeficiency Virus Type-1 subtype C infection.Retrovirology · 2008Article
- Variation in HIV-1 R5 macrophage-tropism correlates with sensitivity to reagents that block envelope: CD4 interactions but not with sensitivity to other entry inhibitors.Retrovirology · 2008Article
- Variation of macrophage tropism among HIV-1 R5 envelopes in brain and other tissues.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2007Review
- Non-macrophage-tropic human immunodeficiency virus type 1 R5 envelopes predominate in blood, lymph nodes, and semen: implications for transmission and pathogenesis.Journal of virology · 2006Article
- Article
- Induction of autoantibodies to CCR5 in macaques and subsequent effects upon challenge with an R5-tropic simian/human immunodeficiency virus.Journal of virology · 2004Article
- Impact of cytokines on replication in the thymus of primary human immunodeficiency virus type 1 isolates from infants.Journal of virology · 2002Article
- HIV-1 escape from a small molecule, CCR5-specific entry inhibitor does not involve CXCR4 use.Proceedings of the National Academy of Sciences of the United States of America · 2002Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Human immunodeficiency virus type 1 (HIV-1) non-syncytium-inducing (NSI) strains predominantly use the chemokine receptor CCR5, while syncytium-inducing (SI) strains use CXCR4. In vitro, SI isolates infect and replicate in a range of CD4(+) CXCR4(+) T-cell lines, whereas NSI isolates usually do not. Here we describe three NSI strains that are able to infect two CD4(+) T-cell lines, Molt4 and SupT1. For one strain, a variant of JRCSF selected in vitro, replication on Molt4 was previously shown to be conferred by a single amino-acid change in the V1 loop (M.T. Boyd et al., J. Virol. 67:3649-3652, 1993). On CD4(+) cell lines expressing different coreceptors, these strains use CCR5 predominantly and do not replicate in CCR5-negative peripheral blood mononuclear cells derived from individuals homozygous for Delta32 CCR5. Furthermore, infection of Molt4 and SupT1 by each of these three strains is potently inhibited by ligands for CCR5, including 2D7, a monoclonal antibody specific for CCR5. CCR5 mRNA was present in both Molt4 and SupT1 by reverse transcription-PCR, although CCR5 protein could not be detected either on the cell surface or in intracellular vesicles. The expanded tropism of the three strains shown here is therefore not due to adaptation to a new coreceptor but due to the capacity to exploit extremely low levels of CCR5 on Molt4 and SupT1 cells. This novel tropism observed for a subset of primary HIV-1 isolates may represent an extended tropism to new CD4(+) cell types in vivo.
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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.