ReviewCurrent HIV/AIDS reports2012
The HIV-1 env protein: a coat of many colors.
Review in Current HIV/AIDS reports, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled it.
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
56 citing papers in PubMed, 1 synthesis or guideline pooled it, 97 citations in OpenAlex.
- Challenges in Elucidating HIV-1 Genetic Diversity in the Middle East and North Africa: A Review Based on a Systematic Search.Viruses · 2025Pooled it
- ViralMap: predicting features in viral proteins from primary sequence.Journal of virology · 2026Article
- Analysis of temporal virus evolution and intra-host diversity in long-term non-progressors by bulk next-generation sequencing.Microbiology spectrum · 2026Article
- Real-world Prevalence of Nonintegrase INSTI Resistance-Associated Mutations and Virological Outcomes in People Who Have Recently Acquired HIV-1 in the United Kingdom.The Journal of infectious diseases · 2026Article
- Modulation of transferrin receptor by HIV-2.Virology journal · 2025Article
- Python-driven impedance profiling on peptide-functionalized biosensor for detection of HIV gp41 envelope protein.3 Biotech · 2025Article
- Mechanisms of Immune Evasion in HIV-1: The Role of Virus-Host Protein Interactions.Current issues in molecular biology · 2025Review
- Passive Immunization in the Prevention and Treatment of Viral Infections.European journal of immunology · 2025Review
- The Role of Peptides in Combatting HIV Infection: Applications and Insights.Molecules (Basel, Switzerland) · 2024Review
- Review
- Article
- Impedimetric antimicrobial peptide biosensor for the detection of human immunodeficiency virus envelope protein gp120.iScience · 2024Article
- The Question of HIV Vaccine: Why Is a Solution Not Yet Available?Journal of immunology research · 2024Review
- Article
- Cell-to-Cell Transmission of HIV-1 and HIV-2 from Infected Macrophages and Dendritic Cells to CD4+ T Lymphocytes.Viruses · 2023Article
- Biotypes of Central Nervous System Complications in People With Human Immunodeficiency Virus: Virology, Immunology, and Neuropathology.The Journal of infectious diseases · 2023Article
- The initial interplay between HIV and mucosal innate immunity.Frontiers in immunology · 2023Review
- Peptide Triazole Inhibitors of HIV-1: Hijackers of Env Metastability.Current protein & peptide science · 2023Review
- Glycan masking in vaccine design: Targets, immunogens and applications.Frontiers in immunology · 2023Review
- Distinct HIV-1 Population Structure across Meningeal and Peripheral T Cells and Macrophage Lineage Cells.Microbiology spectrum · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
HIV-1 is completely dependent upon the Env protein to enter cells. The virus typically replicates in activated CD4+ T cells due to viral entry requirements for the CCR5 coreceptor and for high surface levels of the CD4 receptor. This is the case for the transmitted virus and for most of the virus sampled in the blood. Over the course of infection, the env gene can evolve to encode a protein with altered receptor and coreceptor usage allowing the virus to enter alternative host cells. In about 50% of HIV-1 infections, the viral population undergoes coreceptor switching, usually late in disease, allowing the virus to use CXCR4 to enter a different subset of CD4+ T cells. Neurocognitive disorders occur in about 10% of infections, also usually late in disease, but caused (ultimately) by viral replication in the brain either in CD4+ T cells or macrophage and/or microglia. Expanded host range is significantly intertwined with pathogenesis. Identification and characterization of such HIV-1 variants may be useful for early detection which would allow intervention to reduce viral pathogenesis in these alternative cell types.
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.