Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA189181 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:This study is complementary to the "Genome-wide analysis of host mRNA translation during hepatitis C virus infection" study (GSE44210), for which sucrose gradient ultracentrifugation followed by microarray analysis was used to identify translationally-regulated mRNAs (mRNAs associated with ribosomes) from JFH1-infected and uninfected Huh-7.5.1 cells. MicroRNA arrays have been conducted in parallel on total RNA from infected and uninfected cells, in order to determine if microRNA regulation could explain some of the mRNA translation regulations.
2013-02-17 | GSE44369 | GEO
Project description:This study is complementary to the "Genome-wide analysis of host mRNA translation during hepatitis C virus infection" study (GSE44210), for which sucrose gradient ultracentrifugation followed by microarray analysis was used to identify translationally-regulated mRNAs (mRNAs associated with ribosomes) from JFH1-infected and uninfected Huh-7.5.1 cells. MicroRNA arrays have been conducted in parallel on total RNA from infected and uninfected cells, in order to determine if microRNA regulation could explain some of the mRNA translation regulations. Huh7 cells were infected with HCV JFH-1 strain. Controls consisted in non-infected cells. 3 days after infection, total RNAs were extracted from cell lysate and subjected to miRNA microarray analysis.
2013-02-17 | E-GEOD-44369 | biostudies-arrayexpress
Project description:MiRNA analysis during hepatitis C virus infection
| PRJNA189657 | ENA
Project description:The RNA modification N6-methyladenosine (m6A) can modulate mRNA fate and thus affect many biological processes. We analyzed m6A modification across the transcriptome following infection by dengue virus (DENV), Zika virus (ZIKV), West Nile virus (WNV), and hepatitis C virus (HCV). We found that infection by these viruses in the Flaviviridae family alters m6A modification of specific cellular transcripts, including RIOK3 and CIRBP. During viral infection, the addition of m6A to RIOK3 promotes its translation, while loss of m6A in CIRBP promotes alternative splicing. Importantly, we found that viral activation of innate immune sensing or the endoplasmic reticulum (ER) stress response contributes to the changes in m6A modification in RIOK3 and CIRBP, respectively. Further, several transcripts with infection-altered m6A profiles, including RIOK3 and CIRBP, encode proteins that influence DENV, ZIKV, and HCV infection. Overall, this work reveals that cellular signaling pathways activated during viral infection lead to alterations in m6A modification of host mRNAs to regulate infection.
2019-10-11 | GSE138730 | GEO
Project description:Ribosomes are highly abundant cellular machines that perform the essential task of translating the genetic code into proteins. Cellular translation activity is finely tuned and proteostasis insults, such as those incurred upon viral infection, activate stress signaling pathways that result in translation reprogramming. Viral infection selectively shuts down host mRNA while redistributing ribosomes for selective translation of viral mRNAs. The intricacies of this selective ribosome shuffle from host to viral mRNAs are poorly understood. Here, we uncover a role for the ribosome associated quality control (RQC) factor ZNF598, a sensor for collided ribosomes, as a critical factor for vaccinia virus mRNA translation. Collided ribosomes are sensed by ZNF598, which ubiquitylates 40S subunit proteins uS10 and eS10 and thereby initiates RQC-dependent nascent chain degradation and ribosome recycling. We show that vaccinia infection in human cells enhances uS10 ubiquitylation indicating an increased burden on RQC pathways during viral propagation. Consistent with an increased RQC demand, we demonstrate that vaccinia virus replication is impaired in cells which either lack ZNF598 or contain a ubiquitylation deficient version of uS10. Using SILAC-based proteomics and concurrent RNAseq analysis, we determine that host translation of vaccinia virus mRNAs is compromised in cells that lack RQC activity as compared to control cells whereas there was little evidence of differences in host or viral transcription. Additionally, vaccinia virus infection resulted in a loss of cellular RQC activity, suggesting that ribosomes engaged in viral protein production recruit ZNF598 away from its function in host translation. Thus, co-option of ZNF598 by vaccinia virus plays a critical role in translational reprogramming that is needed for optimal viral propagation.
2021-01-05 | MSV000086660 | MassIVE
Project description:This is a within-host hepatitis B viral mathematical model for hepatitis B in the acute phase of infection. The model incorporates hepatocytes, hepatitis B virus, immune system cells and cytokine dynamics using a system of ordinary differential equations.
2024-12-09 | MODEL1911280002 | BioModels
Project description:Hepatitis C Virus protein NS5A was found to upregulate assembly of cap binding initiation complex eIF4F in Huh7.5 cells. NS5A also was found to associate with translation machinery. To understand consequences of NS5A mediation in host translation, we analyzed mRNA associated with polysome fractions of NS5A expressing Huh7.5 cells and compared them with the corresponding fractions from control cells. Agilent-027114 Genotypic Technology designed Custom Human Whole Genome 8x60k Microarray
2014-05-01 | E-GEOD-46273 | biostudies-arrayexpress
Project description:Hepatitis C Virus protein NS5A was found to upregulate assembly of cap binding initiation complex eIF4F in Huh7.5 cells. NS5A also was found to associate with translation machinery. To understand consequences of NS5A mediation in host translation, we analyzed mRNA associated with polysome fractions of NS5A expressing Huh7.5 cells and compared them with the corresponding fractions from control cells.
2014-05-01 | GSE46273 | GEO
Project description:Here, we examined the host response relative of SACC-PHHs infected with either hepatitis B virus (HBV) alone or both HBV/hepatitis delta virus (HDV) co-infection compared to non-infected controls.
2019-06-18 | GSE112118 | GEO