ArticleVirology2016
Access of HIV-2 to CD169-dependent dendritic cell-mediated trans infection pathway is attenuated.
Article in Virology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed, 9 citations in OpenAlex.
- Role of Siglecs in viral infections: A double-edged sword interaction.Molecular aspects of medicine · 2023Review
- CD169-mediated restrictive SARS-CoV-2 infection of macrophages induces pro-inflammatory responses.PLoS pathogens · 2022Article
- CD169-mediated restrictive SARS-CoV-2 infection of macrophages induces pro-inflammatory responses.bioRxiv : the preprint server for biology · 2022Article
- Dissemination ofJournal of extracellular vesicles · 2021Article
- HIV-2-Infected Macrophages Produce and Accumulate Poorly Infectious Viral Particles.Frontiers in microbiology · 2020Article
- In Vivo Imaging-Driven Approaches to Study Virus Dissemination and Pathogenesis.Annual review of virology · 2019Review
- A Protective Role for the Lectin CD169/Siglec-1 against a Pathogenic Murine Retrovirus.Cell host & microbe · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
The mechanisms behind the low viral loads and lower mortality rates of HIV-2(+) individuals remain unknown. We hypothesized that reduced interaction of HIV-2 with CD169, the primary HIV-1 attachment factor on monocyte-derived dendritic cells (DCs) that targets captured virus particles to the trans infection pathway, contributes to its diminished pathogenic phenotype in vivo. We observed a significant decrease in capture of HIV-2 Gag-eGFP virus-like particles (VLPs) and infectious GFP-containing HIV-2 particles compared to corresponding HIV-1 particles by CD169(+) mature DCs. Interestingly, there was decreased co-localization of HIV-2 with HIV-1 Gag at plasma membrane microdomains in virus producer cells which correlated with reduced incorporation of GM3, the CD169 ligand, in HIV-2 virions, and reduction in mature DC-mediated HIV-2 trans infection compared to HIV-1. We conclude that limited interaction of HIV-2 with CD169 diminishes virus access to the mature DC-mediated trans infection pathway and might result in attenuated HIV-2 dissemination in vivo.
Indexed as
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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.