ArticleThe Journal of experimental medicine1998
HIV-1 variation diminishes CD4 T lymphocyte recognition.
Article in The Journal of experimental medicine, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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.
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Who cites it
34 citing papers in PubMed, 70 citations in OpenAlex.
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- A cell-free antigen processing system informs HIV-1 epitope selection and vaccine design.The Journal of experimental medicine · 2023Article
- Limited immune surveillance in lymphoid tissue by cytolytic CD4+ T cells during health and HIV disease.PLoS pathogens · 2018Article
- CD4 TFrontiers in immunology · 2018Review
- Cytotoxic CD4 T Cells-Friend or Foe during Viral Infection?Frontiers in immunology · 2017Review
- Airway Memory CD4(+) T Cells Mediate Protective Immunity against Emerging Respiratory Coronaviruses.Immunity · 2016Article
- HLA Class-II Associated HIV Polymorphisms Predict Escape from CD4+ T Cell Responses.PLoS pathogens · 2015Article
- A CD4+ T cell antagonist epitope down-regulates activating signaling proteins, up-regulates inhibitory signaling proteins and abrogates HIV-specific T cell function.Retrovirology · 2014Article
- Smarter vaccine design will circumvent regulatory T cell-mediated evasion in chronic HIV and HCV infection.Frontiers in microbiology · 2014Article
- Hepatitis C virus adaptation to T-cell immune pressure.TheScientificWorldJournal · 2013Review
- Article
- CD8+ and CD4+ cytotoxic T cell escape mutations precede breakthrough SIVmac239 viremia in an elite controller.Retrovirology · 2012Article
- Lack of association between HLA class II alleles and in vitro replication capacities of recombinant viruses encoding HIV-1 subtype C Gag-protease from chronically infected individuals.Journal of virology · 2012Article
- Interplay between HIV-1 and Host Genetic Variation: A Snapshot into Its Impact on AIDS and Therapy Response.Advances in virology · 2012Article
- Selection-driven immune escape is not a significant factor in the failure of CD4 T cell responses in persistent hepatitis C virus infection.Hepatology (Baltimore, Md.) · 2010Article
- Human immunodeficiency virus type 1 escapes from interleukin-2-producing CD4+ T-cell responses without high-frequency fixation of mutations.Journal of virology · 2009Article
- The first T cell response to transmitted/founder virus contributes to the control of acute viremia in HIV-1 infection.The Journal of experimental medicine · 2009Article
- CD4+ target cell availability determines the dynamics of immune escape and reversion in vivo.Journal of virology · 2008Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Effective long-term antiviral immunity requires specific cytotoxic T lymphocytes and CD4(+) T lymphocyte help. Failure of these helper responses can be a principle cause of viral persistence. We sought evidence that variation in HIV-1 CD4(+) T helper epitopes might contribute to this phenomenon. To determine this, we assayed fresh peripheral blood mononuclear cells from 43 asymptomatic HIV-1(+) patients for proliferative responses to HIV-1 antigens. 12 (28%) showed a positive response, and we went on to map dominant epitopes in two individuals, to p24 Gag restricted by human histocompatibility leukocyte antigen (HLA)-DR1 and to p17 Gag restricted by HLA-DRB52c. Nine naturally occurring variants of the p24 Gag epitope were found in the proviral DNA of the individual in whom this response was detected. All variants bound to HLA-DR1, but three of these peptides failed to stimulate a CD4(+) T lymphocyte line which recognized the index sequence. Antigenic variation was also detected in the p17 Gag epitope; a dominant viral variant present in the patient was well recognized by a specific CD4(+) T lymphocyte line, whereas several natural mutants were not. Importantly, variants detected at both epitopes also failed to stimulate fresh uncultured cells while index peptide stimulated successfully. These results demonstrate that variant antigens arise in HIV-1(+) patients which fail to stimulate the T cell antigen receptor of HLA class II-restricted lymphocytes, although the peptide epitopes are capable of being presented on the cell surface. In HIV-1 infection, naturally occurring HLA class II-restricted altered peptide ligands that fail to stimulate the circulating T lymphocyte repertoire may curtail helper responses at sites where variant viruses predominate.
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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.