Eukaryotic enteric virus infections modulate the host tissue transcriptome
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE168293 | GEO | 2021/03/05
REPOSITORIES: GEO
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Project description:As obligate intracellular parasites, viruses rely heavily on their host cells for their replication, and therefore dysregulate several cellular processes for their benefit. In return, host cells activate multiple signaling pathways to limit viral replication and eradicate viruses. The present study explores the complex interplay between viruses and their host cells through next generation RNA sequencing. The coding transcriptome of human brain-derived U87 cells infected with Kunjin virus, Zika virus, or Yellow Fever virus were compared to the transcriptome of mock-infected cells. Changes in the abundance of several hundred mRNAs were found in each infection. Moreover, the alternative splicing of hundreds of mRNAs was found to be modulated upon viral infection.
2023-06-28 | GSE232504 | GEO
Project description:Although microbiota plays a critical role for the normal development and function of host immune systems, the detail of the influence, especially on those in the large intestine (LI), remains unknown. Here, we performed transcriptome analysis using Affymetrix GeneChip on LI of germ-free (GF) and specific pathogen free (SPF) mice of IQI, an inbred strain established from ICR. Keywords: comparison of the mice with or without enteric flora
2007-06-06 | GSE8006 | GEO
Project description:Although microbiota plays a critical role for the normal development and function of host immune systems, the detail of the influence, especially on those in the large intestine (LI), remains unknown. Here, we performed transcriptome analysis using Affymetrix GeneChip on LI of germ-free (GF) and specific pathogen free (SPF) mice of IQI, an inbred strain established from ICR. Experiment Overall Design: Male germ-free (GF) and specific pathogen-free (SPF) IQI/Jic mice were bred and maintained in the laboratory of Central Institute for Experimental Animals (CIEA, Kawasaki, Kanagwa, Japan). GF mice were housed in a Trexler-type flexible film isolator in a standard germ free state and screened on a weekly basis for germ-free status by sampling feces sterilely and culturing on MRS-agar plates under aerobic and anaerobic conditions. All the GF, SPF, ex-GF mice were kept in a 12: 12-h light/dark cycle and at a temperature of 22+-2 ºC. Nine week old mice (n=3) were sacrificed by cervical dislocation and the colon was dissected (the colon was not divided into proximal and distal sections and was treated as a single intestinal section). Experiment Overall Design: The SPF mice were provided by the Central Institute for Experimental Animals of Japan. These mice were determined free of the following pathogens (by various techniques including culture, microscopic observation, serological test, and PCR): Dermatophytes, Citrobacter rodentium, Pasteurella pneumotropica, Corynebacterium kutscheri, Pseudomonas aeruginosa, Salmonella spp., Staphylococcus aureus, Mycoplasma pulmonis, Corynebacterium kutscheri, Salmonella typhimurium, Clostridium piliforme, Mycoplasma pulmonis, Mouse hepatitis virus, Sendai virus, Ectromelia virus, Lymphocytic c. virus, Hantavirus, Giardia muris, Spironucleus muris, Syphacia spp., Aspiculuris tetraptera, Ectoparasits, Intestinalprotozoa, Pinworm, Pneumocystis carinii, Helicobacter hepaticus, Helicobacter bilis, EDIM virus(Rotavirus), Pneumonia virus of mice, Minute virus of mice, Mouse adenovirus, Mouse cytomegalovirus, Mouse encephalomyelitis virus, Reovirus type3, and CAR bacillus.
2008-06-15 | E-GEOD-8006 | biostudies-arrayexpress
Project description:As obligate intracellular parasites, viruses rely heavily on their host cells for their replication, and therefore dysregulate several cellular processes for their benefit. In return, host cells activate multiple signaling pathways to limit viral replication and eradicate viruses. The present study explores the complex interplay between viruses and their host cells through next generation RNA sequencing as well as mass spectrometry (SILAC).
2023-10-24 | PXD042208 | Pride
Project description:<p>Definition of the human microbiome is an important scientific priority. This study will expand the scope of the investigation to include viruses, which account for a substantial proportion of infectious disease morbidity and mortality, especially in children. The long-term goal of this project is to describe the human virome in children and to investigate its relevance to febrile illnesses in children. The project will also seek to understand the relationship of the immune system to the composition of the virome. Thus, the project's specific aims are 1) To elucidate the spectrum of viruses that can be detected using non-biased, high throughput sequencing on samples of blood, respiratory, and gastrointestinal secretions from healthy children and to use this information as a basis for understanding the role of viruses in acute febrile illnesses without an obvious source, and 2) to investigate the effect of various forms of immunosuppression on the spectrum of viruses detected in children, and to use this information as a basis for understanding the role of viruses in acute febrile illnesses occurring in these children. Our preliminary studies show that diverse viruses can be detected in children having undiagnosed fever. To carry out the specific aims, well children will be enrolled prior to having elective surgery, and febrile otherwise well children will be enrolled from the Emergency Department at St. Louis Children's Hospital. Immunocompromised children will be recruited from hematopoietic stem cell and solid organ transplant clinics, the HIV/AIDS clinic, and the rheumatology/immunology clinic from the same hospital. Children with fever will have samples obtained at the time of the febrile illness and at 1 and 6-month follow-up visits. Selected samples from each study group will be analyzed at the Genome Center at Washington University (GCWU) using next generation 454 high throughput sequencing to detect and sequence all viral sequences present. We anticipate detecting and sequencing a broad range of viruses, including previously unrecognized agents. A variety of techniques will be used to investigate the significance of viruses detected. Virus-specific PCR assays will be used to determine the frequency and extent of viruses detected by sequencing, using the full range of samples collected. Host response to the detected viruses will be investigated using serologic analysis, cytokine profiling, and microarrays to characterize host gene expression. These studies will take advantage of follow-up samples to compare the acute response with the response in the convalescent period. This study will draw upon the expertise and technological assets of one of the world's most powerful sequencing centers to provide the research community with a comprehensive sequence data base of the viruses that are present in children, which can be used to improve our understanding of the causes of febrile illnesses in young children, many of which are currently undiagnosed.</p>
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Project description:The highly pathogenic avian influenza (HPAI) H5N1 viruses continue to circulate in nature and threaten public health. Although several viral determinants and host factors that influence the virulence of HPAI H5N1 viruses in mammals have been identified, the detailed molecular mechanism remains poorly defined and requires further clarification. In our previous studies, we characterized two naturally isolated HPAI H5N1 viruses that had similar viral genomes but differed substantially in their lethality in mice. Here, we explored the molecular determinants and potential mechanism for this difference in virulence. By using reverse genetics, we found that a single amino acid at position 158 of the hemagglutinin (HA) protein substantially affected the systemic replication and pathogenicity of these H5N1 influenza viruses in mice. We further found that the G158N mutation introduced an N-linked glycosylation at sites 158–160 of the HA protein and that this N-linked glycosylation enhanced viral productivity in infected mammalian cells and induced stronger host immune and inflammatory responses to viral infection. These findings further our understanding of the determinants of pathogenicity of H5N1 viruses in mammals.
2016-12-22 | GSE89246 | GEO
Project description:BACKGROUND: 50% to 80% of asthma exacerbations are precipitated by viral upper respiratory tract infections (RTI), yet the influence of viral pathogen diversity on asthma outcomes is poorly understood due to the limited scope and throughput of conventional viral detection methods. METHODS: We investigated the capability of the Virochip, a DNA microarray-based viral detection platform, to characterize the viral diversity in RTIs in asthmatic and non-asthmatic adults. RESULTS: The Virochip detected viruses in a higher proportion of samples (65%) than culture isolation (17%), while exhibiting high concordance (98%), sensitivity (97%) and specificity (98%) with pathogen-specific PCR. A similar spectrum of viruses was identified in the RTIs from each patient subgroup; however, unexpected diversity among the coronaviruses (HCoVs) and HRVs was revealed. All but one of the HCoVs corresponded to the newly-recognized HCoV-NL63 and HCoV-HKU1 viruses, and over 20 different serotypes of HRVs were detected, including a set of 5 divergent isolates that form a distinct genetic subgroup. CONCLUSIONS: The Virochip can detect both known and novel variants of viral pathogens present in RTIs. Given the diversity detected here, larger scale studies will be necessary to determine if particular substrains of viruses confer an elevated risk of asthma exacerbation This SuperSeries is composed of the SubSeries listed below.
2007-11-07 | GSE8053 | GEO
Project description:Host gene expression responses can be used to determine the etiology of acute infection. PBMCs were stimulated with bacterial, viral, and fungal stimuli and then analyzed for differential gene expression utilizing microarrays to derive pathogen class-specific gene expression classifiers of infection. Discovery Cohort: In vitro human PBMC challenges were performed with bacteria (gram postive and gram negative), viruses (4 strains of influenza), and fungi (Cryptococcus and Candida)
2024-09-28 | GSE277848 | GEO
Project description:Replication defective viral genomes (DVGs) generated during virus replication are the primary triggers of antiviral immunity in many infections. However, DVGs also provide viruses with an evolutionary advantage by facilitating virus persistence. Why and how DVGs and the host interact to achieve these two divergent functions remains unknown. We report that DVGs engage a MAVS-mediated antiviral response that promotes apoptosis on highly infected cells while protecting cells dominated by DVGs from death. We find that MAVS signaling leads to the expression of TNF and of the pro-survival TNFR2/TRAF1 proteins. TNF induces apoptosis of infected cells lacking DVGs, while its signaling in cells enriched in DVGs promotes their survival. These results identify DVGs as pivotal for virus-host co-existence and reveal a MAVS-mediated axis that while promoting the death of infected cells, protects those cells producing toxic cytokines from apoptosis, thereby facilitating viral persistence.
2017-08-01 | GSE96774 | GEO
Project description:Removing cellular transfer RNAs (tRNAs), making their cognate codons unreadable, creates a genetic firewall that prevents viral replication and horizontal gene transfer. However, numerous viruses and mobile genetic elements encode parts of the translational apparatus, including tRNAs, potentially rendering a genetic-code-based firewall ineffective. In this paper, we show that such horizontally transferred tRNA genes can enable viral replication in Escherichia coli cells despite the genome-wide lack of three codons and the previously essential cognate tRNAs and release factor 1. By repurposing viral tRNAs, we then develop recoded cells bearing an amino-acid-swapped genetic code that reassigns two of the six serine codons to leucine during translation. This amino-acid-swapped genetic code renders cells completely resistant to viral infections by mistranslating viral proteomes and prevents the escape of synthetic genetic information by engineered reliance on serine codons to produce leucine-requiring proteins. Finally, we also repurpose the third free codon to biocontain this virus-resistant host via dependence on an amino acid not found in nature.
2022-07-08 | MSV000089854 | MassIVE