ArticleProceedings of the National Academy of Sciences of the United States of America2004
Feline immunodeficiency virus targets activated CD4+ T cells by using CD134 as a binding receptor.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
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Who cites it
59 citing papers in PubMed, 100 citations in OpenAlex.
- Feline immunodeficiency virus: current insights into pathogenesis, clinical impact, and advances in treatment and vaccine development.Frontiers in veterinary science · 2025Review
- Review
- Efficacy assessment of antiretroviral drugs against equine infectious anemia virus in vitro.Virus research · 2024Article
- The Late Asymptomatic and Terminal Immunodeficiency Phases in Experimentally FIV-Infected Cats-A Long-Term Study.Viruses · 2023Article
- HIV induces synaptic hyperexcitation via cGMP-dependent protein kinase II activation in the FIV infection model.PLoS biology · 2018Article
- Properties and Functions of Feline Immunodeficiency Virus Gag Domains in Virion Assembly and Budding.Viruses · 2018Review
- Applications of the FIV Model to Study HIV Pathogenesis.Viruses · 2018Review
- Review
- Transmission, Evolution, and Endogenization: Lessons Learned from Recent Retroviral Invasions.Microbiology and molecular biology reviews : MMBR · 2018Review
- FIV vaccine with receptor epitopes results in neutralizing antibodies but does not confer resistance to challenge.NPJ vaccines · 2018Article
- Feline Immunodeficiency Virus Neuropathogenesis: A Model for HIV-Induced CNS Inflammation and Neurodegeneration.Veterinary sciences · 2017Review
- Interplay of Regulatory T Cell and Th17 Cells during Infectious Diseases in Humans and Animals.Frontiers in immunology · 2017Review
- Pathogenesis of oral FIV infection.PloS one · 2017Article
- Article
- Structural insight into equine lentivirus receptor 1.Protein science : a publication of the Protein Society · 2015Article
- Emergence of CD134 cysteine-rich domain 2 (CRD2)-independent strains of feline immunodeficiency virus (FIV) is associated with disease progression in naturally infected cats.Retrovirology · 2014Article
- Mutations in the feline immunodeficiency virus envelope glycoprotein confer resistance to a dominant-negative fragment of Tsg101 by enhancing infectivity and cell-to-cell virus transmission.Biochimica et biophysica acta · 2014Article
- Replacement of the V3 domain in the surface subunit of the feline immunodeficiency virus envelope glycoprotein with the equivalent region of a T cell-tropic human immunodeficiency virus type 1 results in a chimeric surface protein that efficiently binds to CXCR4.AIDS research and human retroviruses · 2014Article
- Understanding the process of envelope glycoprotein incorporation into virions in simian and feline immunodeficiency viruses.Viruses · 2014Review
- Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The major surface glycoprotein of feline immunodeficiency virus (FIV) specifically binds to a 43-kDa glycoprotein expressed on the surface of a subset of T cells in peripheral blood mononuclear cells and IL-2-dependent T cell lines. Binding to this molecule, in conjunction with CXC chemokine receptor (CXCR) 4, is required for productive infection of these cells by primary isolates of FIV. Here, we demonstrate that the 43-kDa molecule is CD134, a receptor for FIV recently identified independently [Shimojima, M., et al. (2004) Science 303, 1192-1195]. Furthermore, we show that CD134 is specifically up-regulated on CD4+ T cells that have been activated by treatment with IL-2 and Con A. CD8+ T cells remained negative for CD134 expression regardless of the activation state. Binding of the FIV major surface glycoprotein on activated CD4+ T cells was observed through direct interaction with CD134 whereas, on activated CD8+ T cells, the binding was CD134-independent and mediated by CXCR4 and, to a lesser extent, heparan sulfate proteoglycans. However, this CD134-independent interaction was not sufficient to render CD8+ T cells permissive to FIV infection, as FIV replicated primarily in activated CD4+ T cells and not in cells negative for CD134 expression. Altogether, our results substantiate that CD134 acts as a primary binding receptor for FIV and explain the specific targeting and depletion of the CD4+ T cell population observed during the course of infection independent of the use of CD4 as a binding receptor/coreceptor.
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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.