ArticleVirus genes2000
MHC class I-subversive gene functions of cytomegalovirus and their regulation by interferons-an intricate balance.
Article in Virus genes, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
7 citing papers in PubMed, 19 citations in OpenAlex.
- Article
- Classical and non-classical MHC I molecule manipulation by human cytomegalovirus: so many targets—but how many arrows in the quiver?Cellular & molecular immunology · 2015Review
- Is HCMV a tumor promoter?Virus research · 2011Review
- Novel Nipah virus immune-antagonism strategy revealed by experimental and computational study.Journal of virology · 2010Article
- Identification of cytomegalovirus-specific cytotoxic T lymphocytes in vitro is greatly enhanced by the use of recombinant virus lacking the US2 to US11 region or modified vaccinia virus Ankara expressing individual viral genes.Journal of virology · 2005Article
- Antigens and immunoevasins: opponents in cytomegalovirus immune surveillance.Nature reviews. Immunology · 2002Review
- Antigen presentation subverted: Structure of the human cytomegalovirus protein US2 bound to the class I molecule HLA-A2.Proceedings of the National Academy of Sciences of the United States of America · 2001Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Multiple glycoproteins of human cytomegalovirus (HCMV) encoded by the genes US2, US3, US6 and US11 interrupt the MHC class I pathway of antigen presentation at distinct checkpoints to avoid recognition of infected cells by cytotoxic CD8+ T lymphocytes. The action of cytokines like interferon (IFN)-gamma, IFN-alpha/beta and tumour necrosis factor alpha (TNF-alpha) compensate for the viral inhibition and restore antigen presentation in HCMV-infected cells. This finding was explained by their effects on cellular rather than viral genes and reflected by an increase in the production, assembly and maturation of MHC class I molecules resulting in an escape of MHC I from viral control. Here we reproduce the IFN-gamma-mediated effect when MHC I-subversive gene functions of HCMV are tested in isolation, but the efficacy of IFN-gamma to restore MHC I surface expression in US2-, US6- and US11-transfectants differs significantly. In addition, in HCMV-infected cells IFN-gamma strongly affects the synthesis of the US6-encoded glycoprotein. Despite the capability of HCMV to block the interferon signaling pathway the IFN-gamma driven enhancement of MHC class I and class II expression remains effective provided that cells are exposed to IFN-gamma before infection. Our findings illustrate a complex interplay between host immune factors and viral immune evasion functions.
Indexed as
Identifiers
11022788W1586979598What OpenQuestion holds
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.