scholarly journals RNA-Seq Based Transcriptome Analysis of the Type I Interferon Host Response upon Vaccinia Virus Infection of Mouse Cells

2017 ◽  
Vol 2017 ◽  
pp. 1-12 ◽  
Author(s):  
Bruno Hernáez ◽  
Graciela Alonso ◽  
Juan Manuel Alonso-Lobo ◽  
Alberto Rastrojo ◽  
Cornelius Fischer ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Surface ◽  
Vaccinia Virus ◽  
Transcriptional Activation ◽  
Host Response ◽  
Type I Interferon ◽  
Cell Signalling ◽  
Transcriptional Level ◽  
Type I ◽  
Rna Seq

Vaccinia virus (VACV) encodes the soluble type I interferon (IFN) binding protein B18 that is secreted from infected cells and also attaches to the cell surface, as an immunomodulatory strategy to inhibit the host IFN response. By using next generation sequencing technologies, we performed a detailed RNA-seq study to dissect at the transcriptional level the modulation of the IFN based host response by VACV and B18. Transcriptome profiling of L929 cells after incubation with purified recombinant B18 protein showed that attachment of B18 to the cell surface does not trigger cell signalling leading to transcriptional activation. Consistent with its ability to bind type I IFN, B18 completely inhibited the IFN-mediated modulation of host gene expression. Addition of UV-inactivated virus particles to cell cultures altered the expression of a set of 53 cellular genes, including genes involved in innate immunity. Differential gene expression analyses of cells infected with replication competent VACV identified the activation of a broad range of host genes involved in multiple cellular pathways. Interestingly, we did not detect an IFN-mediated response among the transcriptional changes induced by VACV, even after the addition of IFN to cells infected with a mutant VACV lacking B18. This is consistent with additional viral mechanisms acting at different levels to block IFN responses during VACV infection.

scholarly journals Transcriptional activation of the mouse Mx gene by type I interferon.

1986 ◽  
Vol 6 (12) ◽  
pp. 4770-4774 ◽  
Author(s):  
P Staeheli ◽  
P Danielson ◽  
O Haller ◽  
J G Sutcliffe
Keyword(s):  
Gene Expression ◽  
Transcriptional Activation ◽  
Type I Interferon ◽  
Type I ◽  
Mrna Synthesis ◽  
Polyadenylated Rna ◽  
Mrna Concentration ◽  
Mouse Cells ◽  
Ifn Treatment

Mouse cells of the Mx+ genotype accumulate Mx mRNA in response to type I interferon (IFN). Nuclear runoff experiments show that IFN stringently regulates Mx gene expression at the level of transcription. Mx mRNA synthesis peaks about 3 h after IFN treatment, and within 5 h, Mx mRNA concentration rises from undetectable levels to about 0.1% of polyadenylated RNA.

Transcriptional activation of the mouse Mx gene by type I interferon

1986 ◽  
Vol 6 (12) ◽  
pp. 4770-4774 ◽  
Author(s):  
P Staeheli ◽  
P Danielson ◽  
O Haller ◽  
J G Sutcliffe
Keyword(s):  
Gene Expression ◽  
Transcriptional Activation ◽  
Type I Interferon ◽  
Type I ◽  
Mrna Synthesis ◽  
Polyadenylated Rna ◽  
Mrna Concentration ◽  
Mouse Cells ◽  
Ifn Treatment

Mouse cells of the Mx+ genotype accumulate Mx mRNA in response to type I interferon (IFN). Nuclear runoff experiments show that IFN stringently regulates Mx gene expression at the level of transcription. Mx mRNA synthesis peaks about 3 h after IFN treatment, and within 5 h, Mx mRNA concentration rises from undetectable levels to about 0.1% of polyadenylated RNA.

Dual transcriptomics to determine interferon-gamma independent host response to intestinal Cryptosporidium parvum infection

2021 ◽  
Author(s):  
Gina M. Gallego-Lopez ◽  
Carolina Mendoza Cavazos ◽  
Andrés M. Tibabuzo Perdomo ◽  
Andrew L. Garfoot ◽  
Roberta M. O’Connor ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cryptosporidium Parvum ◽  
Chronic Infection ◽  
Host Response ◽  
Type I Interferon ◽  
Secondary Infection ◽  
Transcript Abundance ◽  
Type I ◽  
Transcriptomic Response ◽  
Dual Transcriptomics

Animals with a chronic infection of the parasite Toxoplasma gondii are protected against lethal secondary infection with other pathogens. Our group previously determined that soluble T. gondii antigens (STAg) can mimic this protection and be used as a treatment against several lethal pathogens. Because treatments are limited for the parasite Cryptosporidium parvum , we tested STAg as a C. parvum therapeutic. We determined that STAg treatment reduced C. parvum Iowa II oocyst shedding in IFNγ-KO mice. Murine intestinal sections were then sequenced to define the IFNγ independent transcriptomic response to C. parvum infection. Gene Ontology and transcript abundance comparisons showed host immune response and metabolism changes. Transcripts for type I interferon responsive genes were more abundant in C. parvum infected mice treated with STAg. Comparisons between PBS or STAg treatments showed no significant differences in C. parvum gene expression. C. parvum transcript abundance was highest in the ileum and mucin-like glycoproteins and the GDP-fucose transporter were among the most abundant. These results will assist the field in determining both host- and parasite-directed future therapeutic targets.

scholarly journals Transcriptional Profiling and Machine Learning Unveil a Concordant Biosignature of Type I Interferon-Inducible Host Response Across Nasal Swab and Pulmonary Tissue for COVID-19 Diagnosis

2021 ◽  
Vol 12 ◽  
Author(s):  
Cheng Zhang ◽  
Yi-Gang Feng ◽  
Chiwing Tam ◽  
Ning Wang ◽  
Yibin Feng
Keyword(s):  
Machine Learning ◽  
Lung Tissue ◽  
Host Response ◽  
Nasal Swab ◽  
Type I Interferon ◽  
False Negative ◽  
Transcriptional Profile ◽  
Diagnostic Methods ◽  
Transcriptional Level ◽  
Type I

BackgroundCOVID-19, caused by SARS-CoV-2 virus, is a global pandemic with high mortality and morbidity. Limited diagnostic methods hampered the infection control. Since the direct detection of virus mainly by RT-PCR may cause false-negative outcome, host response-dependent testing may serve as a complementary approach for improving COVID-19 diagnosis.ObjectiveOur study discovered a highly-preserved transcriptional profile of Type I interferon (IFN-I)-dependent genes for COVID-19 complementary diagnosis.MethodsComputational language R-dependent machine learning was adopted for mining highly-conserved transcriptional profile (RNA-sequencing) across heterogeneous samples infected by SARS-CoV-2 and other respiratory infections. The transcriptomics/high-throughput sequencing data were retrieved from NCBI-GEO datasets (GSE32155, GSE147507, GSE150316, GSE162835, GSE163151, GSE171668, GSE182569). Mathematical approaches for homological analysis were as follows: adjusted rand index-related similarity analysis, geometric and multi-dimensional data interpretation, UpsetR, t-distributed Stochastic Neighbor Embedding (t-SNE), and Weighted Gene Co-expression Network Analysis (WGCNA). Besides, Interferome Database was used for predicting the transcriptional factors possessing IFN-I promoter-binding sites to the key IFN-I genes for COVID-19 diagnosis.ResultsIn this study, we identified a highly-preserved gene module between SARS-CoV-2 infected nasal swab and postmortem lung tissue regulating IFN-I signaling for COVID-19 complementary diagnosis, in which the following 14 IFN-I-stimulated genes are highly-conserved, including BST2, IFIT1, IFIT2, IFIT3, IFITM1, ISG15, MX1, MX2, OAS1, OAS2, OAS3, OASL, RSAD2, and STAT1. The stratified severity of COVID-19 may also be identified by the transcriptional level of these 14 IFN-I genes.ConclusionUsing transcriptional and computational analysis on RNA-seq data retrieved from NCBI-GEO, we identified a highly-preserved 14-gene transcriptional profile regulating IFN-I signaling in nasal swab and postmortem lung tissue infected by SARS-CoV-2. Such a conserved biosignature involved in IFN-I-related host response may be leveraged for COVID-19 diagnosis.

#24 Catecholamines enhance viral replication by inhibiting Type I interferon gene expression

2005 ◽  
Vol 19 (4) ◽  
pp. e12-e13
Author(s):  
Alicia Collado-Hidalgo ◽  
Caroline Y. Sung ◽  
Steve W. Cole
Keyword(s):  
Gene Expression ◽  
Viral Replication ◽  
Type I Interferon ◽  
Type I ◽  
Interferon Gene

Factors Involved in the Regulation of Type I Collagen Gene Expression: Implication in Fibrosis

2002 ◽  
Vol 227 (5) ◽  
pp. 301-314 ◽  
Author(s):  
Asish K. Ghosh
Keyword(s):  
Gene Expression ◽  
Collagen Synthesis ◽  
Molecular Mechanisms ◽  
Type I Collagen ◽  
Regulatory Elements ◽  
Transcriptional Level ◽  
Type I ◽  
Collagen Gene ◽  
Cis Acting ◽  
Collagen Gene Expression

Type I collagen, the major component of extracellular matrix in skin and other tissues, is a heterotrimer of two α1 and one α2 collagen polypeptides. The synthesis of both chains is highly regulated by different cytokines at the transcriptional level. Excessive synthesis and deposition of collagen in the dermal region causes thick and hard skin, a clinical manifestation of scleroderma. To better understand the causes of scleroderma or other tissue fibrosis, it is very Important to investigate the molecular mechanisms that cause upregulation of the Type I collagen synthesis in these tissues. Several cis-acting regulatory elements and trans-acting protein factors, which are involved in basal as well as cytokine-modulated Type I collagen gene expression, have been identified and characterized. Hypertranscription of Type I collagen in scleroderma skin fibroblasts may be due to abnormal activities of different positive or negative transcription factors In response to different abnormally induced signaling pathways. In this review, I discuss the present day understanding about the involvement of different factors in the regulation of basal as well as cytokine-modulated Type I collagen gene expression and its implication in scleroderma research.

scholarly journals KAP1 regulates type I interferon/STAT1-mediated IRF-1 gene expression

2008 ◽  
Vol 370 (2) ◽  
pp. 366-370 ◽  
Author(s):  
Shinya Kamitani ◽  
Norihiko Ohbayashi ◽  
Osamu Ikeda ◽  
Sumihito Togi ◽  
Ryuta Muromoto ◽  
...  
Keyword(s):  
Gene Expression ◽  
Type I Interferon ◽  
Type I
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