ArticlePLoS pathogens2019
HLA-B locus products resist degradation by the human cytomegalovirus immunoevasin US11.
Article in PLoS pathogens, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 19 citations in OpenAlex.
- Article
- The human cytomegalovirus-encoded pUS28 antagonizes CD4+ T cell recognition by targeting CIITA.eLife · 2025Article
- B4GALT5 inhibits CD8Journal for immunotherapy of cancer · 2025Article
- Review
- Rhesus Cytomegalovirus-encoded Fcγ-binding glycoproteins facilitate viral evasion from IgG-mediated humoral immunity.Nature communications · 2025Article
- Multimodal HLA-I genotype regulation by human cytomegalovirus US10 and resulting surface patterning.eLife · 2024Article
- Diverse cytomegalovirus US11 antagonism and MHC-A evasion strategies reveal a tit-for-tat coevolutionary arms race in hominids.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Identification of novel canonical and cryptic HCMV-specific T-cell epitopes for HLA-A∗03 and HLA-B∗15 via peptide-PRISM.Blood advances · 2024Article
- Review
- Deciphering the Potential Coding of Human Cytomegalovirus: New Predicted Transmembrane Proteome.International journal of molecular sciences · 2022Article
- Targeting the latent human cytomegalovirus reservoir for T-cell-mediated killing with virus-specific nanobodies.Nature communications · 2021Article
- Identification of HCMV-derived T cell epitopes in seropositive individuals through viral deletion models.The Journal of experimental medicine · 2020Article
- Assessing Anti-HCMV Cell Mediated Immune Responses in Transplant Recipients and Healthy Controls Using a Novel Functional Assay.Frontiers in cellular and infection microbiology · 2020Article
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To escape CD8+ T-cell immunity, human cytomegalovirus (HCMV) US11 redirects MHC-I for rapid ER-associated proteolytic degradation (ERAD). In humans, classical MHC-I molecules are encoded by the highly polymorphic HLA-A, -B and -C gene loci. While HLA-C resists US11 degradation, the specificity for HLA-A and HLA-B products has not been systematically studied. In this study we analyzed the MHC-I peptide ligands in HCMV-infected cells. A US11-dependent loss of HLA-A ligands was observed, but not of HLA-B. We revealed a general ability of HLA-B to assemble with β2m and exit from the ER in the presence of US11. Surprisingly, a low-complexity region between the signal peptide sequence and the Ig-like domain of US11, was necessary to form a stable interaction with assembled MHC-I and, moreover, this region was also responsible for changing the pool of HLA-B ligands. Our data suggest a two-pronged strategy by US11 to escape CD8+ T-cell immunity, firstly, by degrading HLA-A molecules, and secondly, by manipulating the HLA-B ligandome.
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