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    A systems immunology approach to plasmacytoid dendritic cell function in cytopathic virus infections. / G. Bocharov, R. Züst, L. Cervantes-Barragan [et al.] // PLOS pathogens. - 2010. - Vol. 6, № 7. - P1-15 : рис., a-табл. - Bibliogr. : p. 14-15 (52 ref.)

ББК 61
Рубрики: ЗДРАВООХРАНЕНИЕ. МЕДИЦИНСКИЕ НАУКИ
Кл.слова (ненормированные):
ANTIVIRUS AGENT -- DENDRITIC CELL -- ALLERGY AND IMMUNOLOGY
Аннотация: Plasmacytoid dendritic cell (pDC)-mediated protection against cytopathic virus infection involves various molecular, cellular, tissue-scale, and organism-scale events. In order to better understand such multiscale interactions, we have implemented a systems immunology approach focusing on the analysis of the structure, dynamics and operating principles of virus-host interactions which constrain the initial spread of the pathogen. Using high-resolution experimental data sets coming from the well-described mouse hepatitis virus (MHV) model, we first calibrated basic modules including MHV infection of its primary target cells, i.e. pDCs and macrophages (Mphis). These basic building blocks were used to generate and validate an integrative mathematical model for in vivo infection dynamics. Parameter estimation for the system indicated that on a per capita basis, one infected pDC secretes sufficient type I IFN to protect 10(3) to 10(4) Mphis from cytopathic viral infection. This extremely high protective capacity of pDCs secures the spleen's capability to function as a 'sink' for the virus produced in peripheral organs such as the liver. Furthermore, our results suggest that the pDC population in spleen ensures a robust protection against virus variants which substantially down-modulate IFN secretion. However, the ability of pDCs to protect against severe disease caused by virus variants exhibiting an enhanced liver tropism and higher replication rates appears to be rather limited. Taken together, this systems immunology analysis suggests that antiviral therapy against cytopathic viruses should primarily limit viral replication within peripheral target organs

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    Checking gene expression profile associated with IRF7 and UNC93B deficient patient peripheral blood mononuclear cells infected with pH1N1 influenza virus / K. Shinwari, G. Liu, M. A. Bolkov [et al.] // AIP Conference Proceedings. - 2022. - Vol. 2390, № 1. - Ст. 030089
Рубрики: ЗДРАВООХРАНЕНИЕ. МЕДИЦИНСКИЕ НАУКИ
Кл.слова (ненормированные):
VIRUSES -- MICROARRAYS -- GENOMICS
Аннотация: An innate immune defect is a defect in the innate immune response that reduces the response to infection, this can occurs in genes important for activation regulation and proliferation of the innate immune cells or pathways important for the function of innate immunity. The purpose of this study was to identify novel biomarkers of interferon Receptor 7 through bioinformatics analysis and elucidate the possible molecular mechanism. The GSE 66486 datasets containing microarray data from IRF7 and UNC93B patients and healthy controls were downloaded from the GEO database and analyzed by the GEO2R web tool to obtain different expressed genes (DEGs). Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis, protein-protein interaction (PPI), and Biological Networks Gene Oncology tool (BiNGO) were then performed to elucidate the molecular mechanism of IRF7. A total of 490 DEGs were identified, of which 14 were hub genes, and involved in ribosome biogenesis, rRNA processing, gene expression, mRNA processing, nuclear lumen, intracellular non-membrane-bounded organelle, nucleoplasm, small-subunit processome, antigen processing and presentation pathway, and ribosome biogenesis in eukaryotes. Antigen processing and presentation pathway, and ribosome biogenesis in eukaryotes possibly form the basis of IRF7 or UNC93B disorders, while our study provides a list of genes and pathways that are disrupted in IRF7/UNC93B, which has the potential to be used in the clinic for diagnosis and targeted therapy of such disorders in future.

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