ArticlePLoS pathogens2010
HIV-1 envelope subregion length variation during disease progression.
Article in PLoS pathogens, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 1 of them a synthesis that pooled it.
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Who cites it
67 citing papers in PubMed, 1 synthesis or guideline pooled it, 93 citations in OpenAlex.
- Is the virulence of HIV changing? A meta-analysis of trends in prognostic markers of HIV disease progression and transmission.AIDS (London, England) · 2012Pooled it
- CRISPR/Cas9-Based Genome Editing: Understanding Differences in DNA Repair Pathways, Profiles, and Outcomes.International journal of molecular sciences · 2026Review
- Genotypic and phenotypic characteristics of CXCR4-using transmitted/founder HIV-1 envelope glycoproteins.Journal of virology · 2026Article
- Genotypic challenges in implementing broadly neutralizing antibody-based long-acting HIV-1 therapies.Communications medicine · 2026Review
- Germline-somatic residue synergy reshapes antibody encounter-state pathways to enhance HIV-1 recognition.bioRxiv : the preprint server for biology · 2026Article
- Review
- Unique molecular signatures in rebound viruses from antiretroviral drug and CRISPR-treated HIV-1-infected humanized mice.Communications biology · 2025Article
- Article
- Unveiling conserved HIV-1 open reading frames encoding T cell antigens using ribosome profiling.Nature communications · 2025Article
- Rare twin cysteine residues in the HIV-1 envelope variable region 1 link to neutralization escape and breadth development.Cell host & microbe · 2025Article
- The Question of HIV Vaccine: Why Is a Solution Not Yet Available?Journal of immunology research · 2024Review
- Neutralization profiles of HIV-1 viruses from the VRC01 Antibody Mediated Prevention (AMP) trials.PLoS pathogens · 2023Article
- Ongoing HIV-1 evolution and reservoir reseeding in two elite controllers with genetically diverse peripheral proviral quasispecies.Memorias do Instituto Oswaldo Cruz · 2023Article
- Article
- Contribution of the HIV-1 Envelope Glycoprotein to AIDS Pathogenesis and Clinical Progression.Biomedicines · 2022Review
- Analysis of two cooperating antibodies unveils immune pressure imposed on HIV Env to elicit a V3-glycan supersite broadly neutralizing antibody lineage.Frontiers in immunology · 2022Article
- The Characteristics of the HIV-1 Env Glycoprotein Are Linked With Viral Pathogenesis.Frontiers in microbiology · 2022Article
- Limited Evidence for a Relationship between HIV-1 Glycan Shield Features in Early Infection and the Development of Neutralization Breadth.Journal of virology · 2021Article
- SARS-CoV-2 Portrayed against HIV: Contrary Viral Strategies in Similar Disguise.Microorganisms · 2021Review
- Deficient uracil base excision repair leads to persistent dUMP in HIV proviruses during infection of monocytes and macrophages.PloS one · 2020Article
7 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
8 authors at 1 institution in 1 country.
Funding
Abstract
The V3 loop of the HIV-1 Env protein is the primary determinant of viral coreceptor usage, whereas the V1V2 loop region is thought to influence coreceptor binding and participate in shielding of neutralization-sensitive regions of the Env glycoprotein gp120 from antibody responses. The functional properties and antigenicity of V1V2 are influenced by changes in amino acid sequence, sequence length and patterns of N-linked glycosylation. However, how these polymorphisms relate to HIV pathogenesis is not fully understood. We examined 5185 HIV-1 gp120 nucleotide sequence fragments and clinical data from 154 individuals (152 were infected with HIV-1 Subtype B). Sequences were aligned, translated, manually edited and separated into V1V2, C2, V3, C3, V4, C4 and V5 subregions. V1-V5 and subregion lengths were calculated, and potential N-linked glycosylation sites (PNLGS) counted. Loop lengths and PNLGS were examined as a function of time since infection, CD4 count, viral load, and calendar year in cross-sectional and longitudinal analyses. V1V2 length and PNLGS increased significantly through chronic infection before declining in late-stage infection. In cross-sectional analyses, V1V2 length also increased by calendar year between 1984 and 2004 in subjects with early and mid-stage illness. Our observations suggest that there is little selection for loop length at the time of transmission; following infection, HIV-1 adapts to host immune responses through increased V1V2 length and/or addition of carbohydrate moieties at N-linked glycosylation sites. V1V2 shortening during early and late-stage infection may reflect ineffective host immunity. Transmission from donors with chronic illness may have caused the modest increase in V1V2 length observed during the course of the pandemic.
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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.