Host cells infected by various types of viruses
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA145517 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:This SuperSeries is composed of the SubSeries listed below.
2013-01-03 | GSE31524 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series
2013-01-03 | E-GEOD-31524 | biostudies-arrayexpress
Project description:The mechanisms responsible for the molecular pathogenesis of the highly pathogenic avian influenza virus (HPAIV) or low pathogenic avian influenza virus (LPAIV) in avian species remain poorly understood. Thus, global immune response of chickens infected with HPAIV H5N1 (A/duck/India/02CA10/2011) and LPAIV H9N2 (A/duck/India/249800/2010) viruses was studied using microarray to identify crucial host genetic components responsive to these infection. HPAIV H5N1 induced excessive mRNA expression of cytokines (IFNA, OASL, MX1, RSAD2, IFITM5, GBP 1, IL1B, IL18, IL22, IL13, IL12B, CCL4, CCL9, CCL10, CX3CL1 etc) in lung tissues. This excessive cytokine response (cytokine storms) may cause tissue damage and high mortality in chickens. In contrast, the expression levels of most of the cytokines remained unchanged in the lungs of LPAIV H9N2 virus infected chickens. This study indicated the relationship between host cytokines response and their roles in pathogenesis in chickens infected with HPAIVs.
2016-01-02 | GSE65231 | GEO
Project description:The mechanisms responsible for the molecular pathogenesis of the highly pathogenic avian influenza virus (HPAIV) or low pathogenic avian influenza virus (LPAIV) in avian species remain poorly understood. Thus, global immune response of chickens infected with HPAIV H5N1 (A/duck/India/02CA10/2011) and LPAIV H9N2 (A/duck/India/249800/2010) viruses was studied using microarray to identify crucial host genetic components responsive to these infection. HPAIV H5N1 induced excessive mRNA expression of cytokines (IFNA, OASL, MX1, RSAD2, IFITM5, GBP 1, IL1B, IL18, IL22, IL13, IL12B, CCL4, CCL9, CCL10, CX3CL1 etc) in lung tissues. This excessive cytokine response (cytokine storms) may cause tissue damage and high mortality in chickens. In contrast, the expression levels of most of the cytokines remained unchanged in the lungs of LPAIV H9N2 virus infected chickens. This study indicated the relationship between host cytokines response and their roles in pathogenesis in chickens infected with HPAIVs. Agilent Custom Chicken Gene Expression 8X60k (AMADID: G4102A_059389) designed by Genotypic Technology Private Limited , Labeling kit: Agilent Quick-Amp labeling Kit (p/n5190-0442)
2016-07-04 | E-GEOD-65231 | biostudies-arrayexpress
Project description:We isolated two highly pathogenic H5N1 avian influenza viruses (AIVs) (CK10 and GS10) with similar genetic background but greatly differ in pathogencity in mice. CK10 is highly pathogenic in mice, whereas GS10 is nonpathogenic. However, the host mechanism of this differecne in pathogenicity is unclear. We used microarray analysis to evaluate the global transcriptional response in the lung of mice infected with CK10 or GS10.
2012-09-25 | GSE41126 | GEO
Project description:Viral pathogens are an ongoing threat to public health worldwide. Dissecting their dependence on host biosynthetic pathways could lead to effective antiviral therapies. To define how entero- and flaviviruses redirect host ribosomes to synthesize viral proteins and disable host protein production, we performed proteomic analysis of lysates and isolated polysomes from human Huh7 cells infected with either polio, zika or dengue viruses. We find that infection remodels polysome composition along similar principles, without major changes to core ribosome stoichiometry. These viruses use different strategies to evictfrom polysomes a common set of translation initiation and RNA surveillance factors while recruiting host machineries specifically required for viral biogenesis. We also find that both zika and dengue utilize the collagen prolyl-hydroxylation machinery to mediate co-translational modification of conserved prolines in the viral polyprotein. Our findings show how RNA viruses co-opt polysome modularity and establish a powerful strategy to identify targets for selective antiviral interventions.
2021-08-17 | PXD024546 | Pride
Project description:Metagenome of Rubus sp. plants infected/non-infected by viruses Metagenome
| PRJNA1184962 | ENA
Project description:Sequence reads of various foodborne viruses from food
| PRJNA602920 | ENA
Project description:Certain organs are capable of containing the replication of various types of viruses. In the liver, infection of Hepatitis B virus (HBV), the etiological factor of Hepatitis B and hepatocellular carcinoma (HCC), often remains asymptomatic and leads to a chronic carrier state. Here we investigated how hepatocytes contain HBV replication and promote their own survival by orchestrating a translational defense mechanism via the stress-sensitive SUMO-2/3-specific peptidase SENP3. We found that SENP3 expression level decreased in HBV-infected hepatocytes in various models including HepG2-NTCP cell lines and a humanized mouse model. Downregulation of SENP3 reduced HBV replication and boosted host protein translation. We also discovered that IQGAP2, a Ras GTPase-activating-like protein, is a key substrate for SENP3-mediated de-SUMOylation. Downregulation of SENP3 in HBV infected cells facilitated IQGAP2 SUMOylation and degradation, which leads to suppression of HBV gene expression and restoration of global translation of host genes via modulation of AKT phosphorylation. Thus, The SENP3-IQGAP2 de-SUMOylation axis is a host defense mechanism of hepatocytes that restores host protein translation and suppresses HBV gene expression.
2018-11-14 | GSE122461 | GEO
Project description:The determinants of influenza transmission remain poorly understood. Swine influenza viruses preferentially attach to receptors found in the upper airways; however, most swine influenza viruses fail to transmit efficiently from swine to humans, and from human-to-human. The pandemic 2009 H1N1 (H1N1pdm) virus was a rare exception of a swine virus that acquired efficient transmissibility from human-to-human, and is reflected in efficient respiratory droplet transmission in ferrets. We hypothesize that virus-induced host responses in the upper airways correlate with airborne transmission in ferrets. To address this question, we used the H1N1pdm virus and swine influenza A/swine/Hong Kong/201/2010 (HK201) virus that has comparable titre in the ferret nasopharynx, but it exhibits differential transmissibility in ferrets via respiratory droplet route. We performed a transcriptomic analysis of tissues from the upper and lower respiratory tract from ferrets infected with either H1N1pdm or HK201 viruses using ferret-specific Agilent oligonucleotide arrays. We found differences in the kinetics of the innate immune response elicited by these two viruses that varied across tissues.
2017-03-31 | GSE79282 | GEO