ArticleJournal of virology2003
G protein-dependent CCR5 signaling is not required for efficient infection of primary T lymphocytes and macrophages by R5 human immunodeficiency virus type 1 isolates.
Article in Journal of virology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 66 citations in OpenAlex.
- Sustained HIV remission after allogeneic hematopoietic stem cell transplantation with wild-type CCR5 donor cells.Nature medicine · 2024Article
- DNA ultra-sensitive quantification, a technology for studying HIV unintegrated linear DNA.Cell reports methods · 2023Article
- The apparent interferon resistance of transmitted HIV-1 is possibly a consequence of enhanced replicative fitness.PLoS pathogens · 2022Article
- Co-receptor signaling in the pathogenesis of neuroHIV.Retrovirology · 2021Review
- Single-Molecule Super-Resolution Imaging of T-Cell Plasma Membrane CD4 Redistribution upon HIV-1 Binding.Viruses · 2021Article
- Measuring the subcellular compartmentalization of viral infections by protein complementation assay.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- An activator of G protein-coupled receptor and MEK1/2-ERK1/2 signaling inhibits HIV-1 replication by altering viral RNA processing.PLoS pathogens · 2020Article
- Article
- Number of infection events per cell during HIV-1 cell-free infection.Scientific reports · 2017Article
- Δ20 IFITM2 differentially restricts X4 and R5 HIV-1.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Chemoattractant-mediated leukocyte trafficking enables HIV dissemination from the genital mucosa.JCI insight · 2017Article
- Biased small-molecule ligands for selective inhibition of HIV-1 cell entry via CCR5.Pharmacology research & perspectives · 2016Article
- Quantifying the Antiviral Effect of IFN on HIV-1 Replication in Cell Culture.Scientific reports · 2015Article
- Specific cellular incorporation of a pyrene-labelled cholesterol: lipoprotein-mediated delivery toward ordered intracellular membranes.PloS one · 2015Article
- HIV-1 exploits CCR5 conformational heterogeneity to escape inhibition by chemokines.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Use of G-protein-coupled and -uncoupled CCR5 receptors by CCR5 inhibitor-resistant and -sensitive human immunodeficiency virus type 1 variants.Journal of virology · 2013Article
- Constitutively active CCR5 chemokine receptors differ in mediating HIV envelope-dependent fusion.PloS one · 2013Article
- The trinity of the cortical actin in the initiation of HIV-1 infection.Retrovirology · 2012Review
- Allosteric model of maraviroc binding to CC chemokine receptor 5 (CCR5).The Journal of biological chemistry · 2011Article
- Early events of HIV-1 infection: can signaling be the next therapeutic target?Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2011Review
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The requirement of human immunodeficiency virus (HIV)-induced CCR5 activation for infection by R5 HIV type 1 (HIV-1) strains remains controversial. Ectopic CCR5 expression in CD4(+)-transformed cells or pharmacological inhibition of G(alpha)i proteins coupled to CCR5 left unsolved whether CCR5-dependent cell activation is necessary for the HIV life cycle. In this study, we investigated the role played by HIV-induced CCR5-dependent cell signaling during infection of primary CD4-expressing leukocytes. Using lentiviral vectors, we restored CCR5 expression in T lymphocytes and macrophages from individuals carrying the homozygous 32-bp deletion of the CCR5 gene (ccr5 Delta32/Delta32). Expression of wild-type (wt) CCR5 in ccr5 Delta32/Delta32 cells permitted infection by R5 HIV isolates. We assessed the capacity of a CCR5 derivative carrying a mutated DRY motif (CCR5-R126N) in the second intracellular loop to work as an HIV-1 coreceptor. The R126N mutation is known to disable G protein coupling and agonist-induced signal transduction through CCR5 and other G protein-coupled receptors. Despite its inability to promote either intracellular calcium mobilization or cell chemotaxis, the inactive CCR5-R126N mutant provided full coreceptor function to several R5 HIV-1 isolates in primary cells as efficiently as wt CCR5. We conclude that in a primary, CCR5-reconstituted CD4(+) cell environment, G protein signaling is dispensable for R5 HIV-1 isolates to actively infect primary CD4(+) T lymphocytes or macrophages.
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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.