ArticleJournal of virology2009
T-cell tolerance for variability in an HLA class I-presented influenza A virus epitope.
Article in Journal of virology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 28 citations in OpenAlex.
- Molecular basis for universal HLA-A*0201-restricted CD8+ T-cell immunity against influenza viruses.Proceedings of the National Academy of Sciences of the United States of America · 2016Trial
- The contributions of T cell-mediated immunity to protection from vaccine-preventable diseases: A primer.Human vaccines & immunotherapeutics · 2024Review
- Recombinant parainfluenza virus 5 expressing clade 2.3.4.4b H5 hemagglutinin protein confers broad protection against H5Ny influenza viruses.Journal of virology · 2024Article
- Broad CD8Nature communications · 2018Article
- Harnessing the Power of T Cells: The Promising Hope for a Universal Influenza Vaccine.Vaccines · 2018Review
- Impact of Aging and Cytomegalovirus on Immunological Response to Influenza Vaccination and Infection.Frontiers in immunology · 2017Review
- A heat-inactivated H7N3 vaccine induces cross-reactive cellular immunity in HLA-A2.1 transgenic mice.Virology journal · 2016Article
- HLA targeting efficiency correlates with human T-cell response magnitude and with mortality from influenza A infection.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Preemptive priming readily overcomes structure-based mechanisms of virus escape.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Molecular docking analysis of 2009-H1N1 and 2004-H5N1 influenza virus HLA-B*4405-restricted HA epitope candidates: implications for TCR cross-recognition and vaccine development.BMC bioinformatics · 2013Article
- Calreticulin as a hydrophilic chimeric molecular adjuvant enhances IgG responses to the spike protein of severe acute respiratory syndrome coronavirus.Microbiology and immunology · 2012Article
- Engineering temperature sensitive live attenuated influenza vaccines from emerging viruses.Vaccine · 2012Article
- Dynamic variations in the peripheral blood lymphocyte subgroups of patients with 2009 pandemic H1N1 swine-origin influenza A virus infection.Virology journal · 2011Article
- Immunity to seasonal and pandemic influenza A viruses.Microbes and infection · 2011Review
- Protective efficacy of cross-reactive CD8+ T cells recognising mutant viral epitopes depends on peptide-MHC-I structural interactions and T cell activation threshold.PLoS pathogens · 2010Article
- Cross-reactive CD8+ T-cell immunity between the pandemic H1N1-2009 and H1N1-1918 influenza A viruses.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
To escape immune recognition, viruses acquire amino acid substitutions in class I human leukocyte antigen (HLA)-presented cytotoxic T-lymphocyte (CTL) epitopes. Such viral escape mutations may (i) prevent peptide processing, (ii) diminish class I HLA binding, or (iii) alter T-cell recognition. Because residues 418 to 426 of the hypervariable influenza A virus nucleoprotein (NP(418-426)) epitope are consistently bound by class I HLA and presented to CTL, we assessed the impact that intraepitope sequence variability has upon T-cell recognition. CTL elicited by intranasal influenza virus infection were tested for their cross-recognition of 20 natural NP(418-426) epitope variants. Six of the variant epitopes, of both H1N1 and H3N2 origin, were cross-recognized by CTL while the remaining NP(418-426) epitope variants escaped targeting. A pattern emerged whereby variability at position 5 (P5) within the epitope reduced T-cell recognition, changes at P4 or P6 enabled CTL escape, and a mutation at P8 enhanced T-cell recognition. These data demonstrate that substitutions at P4 and/or P6 facilitate influenza virus escape from T-cell recognition and provide a model for the number, nature, and location of viral mutations that influence T-cell cross-recognition.
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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.