ArticlePLoS pathogens2011
CTL escape mediated by proteasomal destruction of an HIV-1 cryptic epitope.
Article in PLoS pathogens, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 36 citations in OpenAlex.
- Non-AUG HIV-1 uORF translation elicits specific T cell immune response and regulates viral transcript expression.Nature communications · 2025Article
- Unveiling conserved HIV-1 open reading frames encoding T cell antigens using ribosome profiling.Nature communications · 2025Article
- Defective HIV-1 genomes and their potential impact on HIV pathogenesis.Retrovirology · 2022Review
- Neddylation of Enterovirus 71 VP2 Protein Reduces Its Stability and Restricts Viral Replication.Journal of virology · 2022Article
- Refining the DC-targeting vaccination for preventing emerging infectious diseases.Frontiers in immunology · 2022Review
- Know thy immune self and non-self: Proteomics informs on the expanse of self and non-self, and how and where they arise.Proteomics · 2021Review
- SARS-CoV-2 Consensus-Sequence and Matching Overlapping Peptides Design for COVID19 Immune Studies and Vaccine Development.Vaccines · 2020Article
- Antigen processing and presentation in HIV infection.Molecular immunology · 2019Review
- Influenza A Virus Infection Induces Viral and Cellular Defective Ribosomal Products Encoded by Alternative Reading Frames.Journal of immunology (Baltimore, Md. : 1950) · 2019Article
- Antisense-Derived HIV-1 Cryptic Epitopes Are Not Major Drivers of Viral Evolution during the Acute Phase of Infection.Journal of virology · 2018Article
- Article
- Two ribosome recruitment sites direct multiple translation events within HIV1 Gag open reading frame.Nucleic acids research · 2017Article
- Presentation of Cryptic Peptides by MHC Class I Is Enhanced by Inflammatory Stimuli.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- Viral infection causes a shift in the self peptide repertoire presented by human MHC class I molecules.Proteomics. Clinical applications · 2015Article
- Immunoproteasomes edit tumors, which then escapes immune recognition.European journal of immunology · 2015Article
- Enhanced Recognition of HIV-1 Cryptic Epitopes Restricted by HLA Class I Alleles Associated With a Favorable Clinical Outcome.Journal of acquired immune deficiency syndromes (1999) · 2015Article
- The HIV-1 antisense protein (ASP) induces CD8 T cell responses during chronic infection.Retrovirology · 2015Article
- Review
- Acute phase CD8+ T lymphocytes against alternate reading frame epitopes select for rapid viral escape during SIV infection.PloS one · 2013Article
- Potential elucidation of a novel CTL epitope in HIV-1 protease by the protease inhibitor resistance mutation L90M.PloS one · 2013Article
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Authors and funding
17 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cytotoxic CD8+ T cells (CTLs) play a critical role in controlling viral infections. HIV-infected individuals develop CTL responses against epitopes derived from viral proteins, but also against cryptic epitopes encoded by viral alternative reading frames (ARF). We studied here the mechanisms of HIV-1 escape from CTLs targeting one such cryptic epitope, Q9VF, encoded by an HIVgag ARF and presented by HLA-B*07. Using PBMCs of HIV-infected patients, we first cloned and sequenced proviral DNA encoding for Q9VF. We identified several polymorphisms with a minority of proviruses encoding at position 5 an aspartic acid (Q9VF/5D) and a majority encoding an asparagine (Q9VF/5N). We compared the prevalence of each variant in PBMCs of HLA-B*07+ and HLA-B*07- patients. Proviruses encoding Q9VF/5D were significantly less represented in HLA-B*07+ than in HLA-B*07- patients, suggesting that Q9FV/5D encoding viruses might be under selective pressure in HLA-B*07+ individuals. We thus analyzed ex vivo CTL responses directed against Q9VF/5D and Q9VF/5N. Around 16% of HLA-B*07+ patients exhibited CTL responses targeting Q9VF epitopes. The frequency and the magnitude of CTL responses induced with Q9VF/5D or Q9VF/5N peptides were almost equal indicating a possible cross-reactivity of the same CTLs on the two peptides. We then dissected the cellular mechanisms involved in the presentation of Q9VF variants. As expected, cells infected with HIV strains encoding for Q9VF/5D were recognized by Q9VF/5D-specific CTLs. In contrast, Q9VF/5N-encoding strains were neither recognized by Q9VF/5N- nor by Q9VF/5D-specific CTLs. Using in vitro proteasomal digestions and MS/MS analysis, we demonstrate that the 5N variation introduces a strong proteasomal cleavage site within the epitope, leading to a dramatic reduction of Q9VF epitope production. Our results strongly suggest that HIV-1 escapes CTL surveillance by introducing mutations leading to HIV ARF-epitope destruction by proteasomes.
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