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  • 1
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    Surface expression of HLA-E, an inhibitor of natural killer cells, enhanced by human cytomegalovirus gpUL40 (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-02-11
    Description: The nonclassical major histocompatibility complex (MHC) class I molecule HLA-E inhibits natural killer (NK) cell-mediated lysis by interacting with CD94/NKG2A receptors. Surface expression of HLA-E depends on binding of conserved peptides derived from MHC class I molecules. The same peptide is present in the leader sequence of the human cytomegalovirus (HCMV) glycoprotein UL40 (gpUL40). It is shown that, independently of the transporter associated with antigen processing, gpUL40 can up-regulate expression of HLA-E, which protects targets from NK cell lysis. While classical MHC class I molecules are down-regulated, HLA-E is up-regulated by HCMV. Induction of HLA-E surface expression by gpUL40 may represent an escape route for HCMV.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tomasec, P -- Braud, V M -- Rickards, C -- Powell, M B -- McSharry, B P -- Gadola, S -- Cerundolo, V -- Borysiewicz, L K -- McMichael, A J -- Wilkinson, G W -- New York, N.Y. -- Science. 2000 Feb 11;287(5455):1031.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of Wales College of Medicine, Cardiff CF14 4XN, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10669413" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Amino Acid Substitution ; *Antigens, CD ; Cell Line ; Cell Membrane/immunology ; Cells, Cultured ; Conserved Sequence ; Cytomegalovirus/genetics/immunology/*metabolism ; Cytotoxicity, Immunologic ; Down-Regulation ; HLA Antigens/immunology/*metabolism ; Histocompatibility Antigens Class I/immunology/*metabolism ; Humans ; Killer Cells, Natural/*immunology ; Molecular Sequence Data ; Open Reading Frames ; Protein Sorting Signals/chemistry/*metabolism ; Receptors, Immunologic/metabolism ; Recombinant Fusion Proteins/chemistry/metabolism ; Transfection ; Up-Regulation ; Viral Proteins/chemistry/genetics/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Complex I binding by a virally encoded RNA regulates mitochondria-induced cell death (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-06-02
    Description: Human cytomegalovirus infection perturbs multiple cellular processes that could promote the release of proapoptotic stimuli. Consequently, it encodes mechanisms to prevent cell death during infection. Using rotenone, a potent inhibitor of the mitochondrial enzyme complex I (reduced nicotinamide adenine dinucleotide-ubiquinone oxido-reductase), we found that human cytomegalovirus infection protected cells from rotenone-induced apoptosis, a protection mediated by a 2.7-kilobase virally encoded RNA (beta2.7). During infection, beta2.7 RNA interacted with complex I and prevented the relocalization of the essential subunit genes associated with retinoid/interferon-induced mortality-19, in response to apoptotic stimuli. This interaction, which is important for stabilizing the mitochondrial membrane potential, resulted in continued adenosine triphosphate production, which is critical for the successful completion of the virus' life cycle. Complex I targeting by a viral RNA represents a refined strategy to modulate the metabolic viability of the infected host cell.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Reeves, Matthew B -- Davies, Andrew A -- McSharry, Brian P -- Wilkinson, Gavin W -- Sinclair, John H -- G0700142/Medical Research Council/United Kingdom -- G9202171/Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2007 Jun 1;316(5829):1345-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of Cambridge, Addenbrooke's Hospital, Hills Road, Cambridge, CB2 2QQ, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17540903" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; *Apoptosis ; Apoptosis Regulatory Proteins/genetics/metabolism ; Cell Line ; Cell Line, Tumor ; Cell Nucleus/metabolism ; Cytomegalovirus/genetics/growth & development/*physiology ; Electron Transport Complex I/antagonists & inhibitors/*metabolism ; Enzyme Inhibitors/pharmacology ; Fibroblasts/metabolism/virology ; Humans ; Membrane Potential, Mitochondrial ; Mitochondria/*metabolism ; NADH, NADPH Oxidoreductases/genetics/metabolism ; Neurons/*cytology/*virology ; Oxidative Stress ; RNA, Untranslated/genetics/metabolism ; RNA, Viral/genetics/*metabolism ; Rotenone/pharmacology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 3
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    Innate immune genes synergize to predict increased risk of chronic disease in hepatitis C virus infection (2011)
    National Academy of Sciences
    Details
    Publication Date: 2011-03-14
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 4
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    Innate immune genes synergize to predict increased risk of chronic disease in hepatitis C virus infection [Immunology] (2011)
    National Academy of Sciences
    Details
    Publication Date: 2011-04-06
    Description: Hepatitis C is a common infection with significant morbidity and mortality, and only a minority of patients successfully clear the infection. Identification of factors that influence disease progression in HCV infection is difficult owing to the lack of well-defined patient cohorts. However, recent evidence supports a role for the innate immune system in virus clearance. In this study, we investigated innate immune genes for their contribution to disease progression in a unique cohort of well-controlled HCV-infected patients. The Irish cohort of HCV patients is uniquely homogenous; patients were infected with a single genotype of HCV from contaminated anti-D Ig. We genotyped 543 infected patients, including 247 patients who spontaneously resolved infection, for natural killer (NK) cell-associated killer cell Ig-like receptors (KIR) genes and the recently reported IL28B (IFNλ3) SNP. The NK cell gene KIR2DS3 was significantly increased in patients with chronic infection [odds ratio (OR) 1.90, 95% confidence interval (CI) 1.25–2.90, P 〈 0.002]. The IL28B “T” allele was also significantly increased in chronically infected patients (OR 7.38, 95% CI 4.93–11.07, P 〈 10−8). The presence of both markers synergized to significantly increase the risk of chronic infection over either factor alone (OR 20.11, 95% CI 9.05–44.68, P 〈 10−7). In functional experiments, we found that IL28A significantly inhibited IFN-γ production by NK cells. Thus, we demonstrate a functional link between NK cells and type 3 IFN. Our findings may contribute to the development of a prognostic test for HCV and identify therapeutic strategies for the clinical management of HCV-infected patients.
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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