ArticleJournal of virology2003
Cell surface expression of major histocompatibility complex class I molecules is reduced in hepatitis C virus subgenomic replicon-expressing cells.
Article in Journal of virology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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
25 citing papers in PubMed, 45 citations in OpenAlex.
- Review
- CXCL14 suppresses human papillomavirus-associated head and neck cancer through antigen-specific CD8Oncogene · 2019Article
- Conserved and variable natural killer cell receptors: diverse approaches to viral infections.Immunology · 2019Review
- Malaria Parasite Liver Infection and Exoerythrocytic Biology.Cold Spring Harbor perspectives in medicine · 2017Review
- Modulation of Human Leukocyte Antigen-C by Human Cytomegalovirus Stimulates KIR2DS1 Recognition by Natural Killer Cells.Frontiers in immunology · 2017Article
- Organ system view of the hepatic innate immunity in HCV infection.Journal of medical virology · 2016Review
- Natural killer cells in hepatitis C: Current progress.World journal of gastroenterology · 2016Review
- Host ER stress during malaria parasite infection.EMBO reports · 2015Article
- Article
- Hepatitis C virus attenuates interferon-induced major histocompatibility complex class I expression and decreases CD8+ T cell effector functions.Gastroenterology · 2014Article
- The effect of bovine viral diarrhea virus (BVDV) strains on bovine monocyte-derived dendritic cells (Mo-DC) phenotype and capacity to produce BVDV.Virology journal · 2014Article
- Hepatitis B virus X protein inhibits autophagic degradation by impairing lysosomal maturation.Autophagy · 2014Article
- A cognitive computational model inspired by the immune system response.BioMed research international · 2014Article
- Influence of HIV and HCV on T cell antigen presentation and challenges in the development of vaccines.Frontiers in microbiology · 2014Review
- Host glycans and antigen presentation.Microbes and infection · 2012Review
- Roles for major histocompatibility complex glycosylation in immune function.Seminars in immunopathology · 2012Review
- Virus-induced ER stress and the unfolded protein response.Frontiers in plant science · 2012Article
- The unfolded protein response (UPR)-activated transcription factor X-box-binding protein 1 (XBP1) induces microRNA-346 expression that targets the human antigen peptide transporter 1 (TAP1) mRNA and governs immune regulatory genes.The Journal of biological chemistry · 2011Article
- Dysfunction of autophagy participates in vacuole formation and cell death in cells replicating hepatitis C virus.Journal of virology · 2011Article
- Cell-to-cell contact with hepatitis C virus-infected cells reduces functional capacity of natural killer cells.Journal of virology · 2011Article
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
Abstract
The hepatitis C virus (HCV) causes chronic hepatitis in most infected individuals by evading host immune defenses. In this investigation, we show that HCV-infected cells may go undetected in the immune system by suppressing major histocompatibility complex (MHC) class I antigen presentation to cytotoxic T lymphocytes. Cells expressing HCV subgenomic replicons have lower MHC class I cell surface expression. This is due to reduced levels of properly folded MHC class I molecules. HCV replicons induce endoplasmic reticulum (ER) stress (K. Tardif, K. Mori, and A. Siddiqui, J. Virol. 76:7453-7459, 2002), which results from a decline in protein glycosylation. Decreasing protein glycosylation can disrupt protein folding, preventing the assembly of MHC class I molecules. This results in the accumulation of unfolded MHC class I. Therefore, the persistence and pathogenesis of HCV may depend upon the ER stress-mediated interference of MHC class I assembly and cell surface expression.
Indexed as
Identifiers
What 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.