ArticleJournal of virology2011
Human cytomegalovirus disrupts the major histocompatibility complex class I peptide-loading complex and inhibits tapasin gene transcription.
Article in Journal of virology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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.
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Who cites it
27 citing papers in PubMed, 50 citations in OpenAlex.
- Article
- Viral manipulation of the HLA class I antigen processing and presentation pathway.Frontiers in immunology · 2025Review
- Conformation of HLA-E/peptide complex guides interaction with two novel HLA-E receptors: Stabilin 1 and 2.PloS one · 2025Article
- Human Fcγ-receptors selectively respond to C-reactive protein isoforms.Frontiers in immunology · 2025Article
- pUS6 in pseudorabies virus participates in the process of inhibiting antigen presentation by inhibiting the assembly of peptide loading complex.BMC veterinary research · 2024Article
- Multimodal HLA-I genotype regulation by human cytomegalovirus US10 and resulting surface patterning.eLife · 2024Article
- Chikungunya virus infection disrupts MHC-I antigen presentation via nonstructural protein 2.PLoS pathogens · 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
- Murine cytomegalovirus downregulates ERAAP and induces an unconventional T cell response to self.Cell reports · 2023Article
- Detection and functional resolution of soluble immune complexes by an FcγR reporter cell panel.EMBO molecular medicine · 2022Article
- Article
- Article
- Presence of donor-encoded centromeric KIR B content increases the risk of infectious mortality in recipients of myeloablative, T-cell deplete, HLA-matched HCT to treat AML.Bone marrow transplantation · 2020Article
- HLA-B locus products resist degradation by the human cytomegalovirus immunoevasin US11.PLoS pathogens · 2019Article
- The complex of MCMV proteins and MHC class I evades NK cell control and drives the evolution of virus-specific activating Ly49 receptors.The Journal of experimental medicine · 2019Article
- Expression of IL-7Rα and KLRG1 defines functionally distinct CD8European journal of immunology · 2019Article
- The polymorphism at residue 156 determines the HLA-B*35 restricted peptide repertoire during HCMV infection.Immunogenetics · 2018Article
- A highly conserved sequence of the viral TAP inhibitor ICP47 is required for freezing of the peptide transport cycle.Scientific reports · 2017Article
- Suppression of human metapneumovirus (HMPV) infection by the innate sensing gene CEACAM1.Oncotarget · 2016Article
- CEACAM1-Mediated Inhibition of Virus Production.Cell reports · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Major histocompatibility complex class I (MHC I) molecules present antigenic peptides for CD8(+) T-cell recognition. Prior to cell surface expression, proper MHC I loading is conducted by the peptide-loading complex (PLC), composed of the MHC I heavy chain (HC) and β(2)-microglobulin (β(2)m), the peptide transporter TAP, and several chaperones, including tapasin. Tapasin connects peptide-receptive MHC I molecules to the PLC, thereby facilitating loading of high-affinity peptides onto MHC I. To cope with CD8(+) T-cell responses, human cytomegalovirus (HCMV) encodes several posttranslational strategies inhibiting peptide transport and MHC I biogenesis which have been studied extensively in transfected cells. Here we analyzed assembly of the PLC in naturally HCMV-infected fibroblasts throughout the protracted replication cycle. MHC I incorporation into the PLC was absent early in HCMV infection. Subsequently, tapasin neosynthesis became strongly reduced, while tapasin steady-state levels diminished only slowly in infected cells, revealing a blocked synthesis rather than degradation. Tapasin mRNA levels were continuously downregulated during infection, while tapasin transcripts remained stable and long-lived. Taking advantage of a novel method by which de novo transcribed RNA is selectively labeled and analyzed, an immediate decline of tapasin transcription was seen, followed by downregulation of TAP2 and TAP1 gene expression. However, upon forced expression of tapasin in HCMV-infected cells, repair of MHC I incorporation into the PLC was relatively inefficient, suggesting an additional level of HCMV interference. The data presented here document a two-pronged coordinated attack on tapasin function by HCMV.
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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.