ArticleThe Journal of clinical investigation2009
The inability to disrupt the immunological synapse between infected human T cells and APCs distinguishes HIV-1 from most other primate lentiviruses.
Article in The Journal of clinical investigation, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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
37 citing papers in PubMed, 55 citations in OpenAlex.
- Ancestral reconstruction supports that loss of Nef-mediated T cell modulation coincided with the emergence of pathogenic lentiviruses.Journal of virology · 2025Article
- Lentiviral Nef Proteins Differentially Govern the Establishment of Viral Latency.Journal of virology · 2022Article
- HIV-1 infection of CD4 T cells impairs antigen-specific B cell function.The EMBO journal · 2020Article
- Loss of Nef-mediated CD3 down-regulation in the HIV-1 lineage increases viral infectivity and spread.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- How HIV Nef Proteins Hijack Membrane Traffic To Promote Infection.Journal of virology · 2019Review
- Masters of manipulation: Viral modulation of the immunological synapse.Cellular microbiology · 2018Review
- Species-specific host factors rather than virus-intrinsic virulence determine primate lentiviral pathogenicity.Nature communications · 2018Article
- Endocytic sorting motif interactions involved in Nef-mediated downmodulation of CD4 and CD3.Nature communications · 2017Article
- HIV-1 Vpu Downmodulates ICAM-1 Expression, Resulting in Decreased Killing of Infected CD4Journal of virology · 2017Article
- Article
- Primate Lentiviruses Modulate NF-κB Activity by Multiple Mechanisms to Fine-Tune Viral and Cellular Gene Expression.Frontiers in microbiology · 2017Review
- HIV Envelope gp120 Alters T Cell Receptor Mobilization in the Immunological Synapse of Uninfected CD4 T Cells and Augments T Cell Activation.Journal of virology · 2016Article
- The KT Jeang Retrovirology prize 2016: Frank Kirchhoff.Retrovirology · 2016Article
- Article
- Lentiviral Nef proteins manipulate T cells in a subset-specific manner.Journal of virology · 2015Article
- Human metapneumovirus SH and G glycoproteins inhibit macropinocytosis-mediated entry into human dendritic cells and reduce CD4+ T cell activation.Journal of virology · 2014Article
- Heterologous Src homology 4 domains support membrane anchoring and biological activity of HIV-1 Nef.The Journal of biological chemistry · 2014Article
- Link between primate lentiviral coreceptor usage and Nef function.Cell reports · 2013Article
- Primate lentiviral Nef proteins deregulate T-cell development by multiple mechanisms.Retrovirology · 2013Article
- HIV-1 Nef and T-cell activation: a history of contradictions.Future virology · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Viruses that infect T cells, including those of the lentivirus genus, such as HIV-1, modulate the responsiveness of infected T cells to stimulation by interacting APCs in a manner that renders the T cells more permissive for viral replication. HIV-1 and other primate lentiviruses use their Nef proteins to manipulate the T cell/APC contact zone, the immunological synapse (IS). It is known that primate lentiviral Nef proteins differ substantially in their ability to modulate cell surface expression of the TCR-CD3 and CD28 receptors critical for the formation and function of the IS. However, the impact of these differences in Nef function on the interaction and communication between virally infected T cells and primary APCs has not been investigated. Here we have used primary human cells to show that Nef proteins encoded by HIV-2 and most SIVs, which downmodulate cell surface expression of TCR-CD3, disrupt formation of the IS between infected T cells and Ag-presenting macrophages or DCs. In contrast, nef alleles from HIV-1 and its simian precursor SIVcpz failed to suppress synapse formation and events downstream of TCR signaling. Our data suggest that most primate lentiviruses disrupt communication between virally infected CD4+ Th cells and APCs, whereas HIV-1 and its SIV precursor have largely lost this capability. The resulting differences in the levels of T cell activation and apoptosis may play a role in the pathogenesis of AIDS.
Indexed as
Identifiers
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.