ArticleJournal of virology2006
Contribution of Vpu, Env, and Nef to CD4 down-modulation and resistance of human immunodeficiency virus type 1-infected T cells to superinfection.
Article in Journal of virology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 132 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
132 citing papers in PubMed, 204 citations in OpenAlex.
- Boosting with AIDSVAX B/E Enhances Env Constant Region 1 and 2 Antibody-Dependent Cellular Cytotoxicity Breadth and Potency.Journal of virology · 2020Trial
- Quantitative and amino acid sequence analysis of soluble HIV-1 Vpu and calmodulin interactions.Protein science : a publication of the Protein Society · 2026Article
- Nef stabilizes actin to prevent HIV-1 sensing by RIG-I-like receptors.Nature communications · 2025Article
- Modulation of transferrin receptor by HIV-2.Virology journal · 2025Article
- The HIV-1 envelope cytoplasmic tail protects infected cells from ADCC by downregulating CD4.mBio · 2025Article
- HIV-1 manipulates CD96 on CD4Science advances · 2025Article
- Assembly of CCR5 with gp120 inhibits the HIV infectivity specifically in T cells.Scientific reports · 2025Article
- Adaptor Protein Complexes in HIV-1 Pathogenesis: Mechanisms and Therapeutic Potential.Viruses · 2025Review
- Impairment of endocytosis-related factors FNBP1L, ARHGAP24, and ATP6V1B1 increases HIV-1 entry into dendritic cells.Journal of virology · 2025Article
- Unveiling conserved HIV-1 open reading frames encoding T cell antigens using ribosome profiling.Nature communications · 2025Article
- Article
- Eilat virus (EILV) causes superinfection exclusion against West Nile virus (WNV) in a strain-specific manner inThe Journal of general virology · 2024Article
- Review
- Differential Ability of Spike Protein of SARS-CoV-2 Variants to Downregulate ACE2.International journal of molecular sciences · 2024Article
- Article
- Potent latency reversal by Tat RNA-containing nanoparticle enables multi-omic analysis of the HIV-1 reservoir.Nature communications · 2023Article
- Advances in HIV Research Using Mass Cytometry.Current HIV/AIDS reports · 2023Review
- Small CD4 mimetics sensitize HIV-1-infected macrophages to antibody-dependent cellular cytotoxicity.Cell reports · 2023Article
- Unique Structure and Distinctive Properties of the Ancient and Ubiquitous Gamma-Type Envelope Glycoprotein.Viruses · 2023Review
- A CRISPR-Cas Cure for HIV/AIDS.International journal of molecular sciences · 2023Review
72 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human immunodeficiency virus type 1 (HIV-1) utilizes Vpu, Env, and Nef to down-modulate its primary CD4 receptor from the cell surface, and this function seems to be critical for the pathogenesis of AIDS. The physiological relevance of CD4 down-modulation, however, is currently not well understood. In the present study, we analyzed the kinetics of CD4 down-modulation and the susceptibility of HIV-1-infected T cells to superinfection using proviral HIV-1 constructs containing individual and combined defects in vpu, env, and nef and expressing red or green fluorescent proteins. T cells infected with HIV-1 mutants containing functional nef genes expressed low surface levels of CD4 from the first moment that viral gene expression became detectable. In comparison, Vpu and Env had only minor to moderate effects on CD4 during later stages of infection. Consistent with these quantitative differences, Nef inhibited superinfection more efficiently than Vpu and Env. Notably, nef alleles from AIDS patients were more effective in preventing superinfection than those derived from a nonprogressor of HIV-1 infection. Our data suggest that protection against X4-tropic HIV-1 superinfection involves both CD4-independent and CD4-dependent mechanisms of HIV-1 Nef. X4 was effectively down-regulated by simian immunodeficiency virus and HIV-2 but not by HIV-1 Nef proteins. Thus, maximal protection seems to involve an as-yet-unknown mechanism that is independent of CD4 or coreceptor down-modulation. Finally, we demonstrate that superinfected primary T cells show enhanced levels of apoptosis. Accordingly, one reason that HIV-1 inhibits CD4 surface expression and superinfection is to prevent premature cell death in order to expand the period of effective virus production.
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.