Enhancement of Chikungunya virus genome replication in mammalian cells at sub-physiological temperatures
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1102705 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR28752900.fastq.gz | Fastqsanger.gz | |||
| SRR28752901.fastq.gz | Fastqsanger.gz | |||
| SRR28752902.fastq.gz | Fastqsanger.gz | |||
| SRR28752903.fastq.gz | Fastqsanger.gz | |||
| SRR28752904.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 45 |
Similar Datasets
Project description:Chikungunya virus (CHIKV) is an Alphavirus transmitted by Aedes mosquitoes, causing fever, rash and arthralgia in mammals. The function of the CHIKV non-structural protein 3 (nsP3) remains enigmatic. Building on previous studies, we generated a panel of mutants in a conserved and surface-exposed cluster in the nsP3 alphavirus unique domain (AUD) and tested their replication using a sub-genomic replicon (SGR). Three of these SGR mutants replicated well in mosquito cells but poorly in mammalian cells. We observed that this difference was due to cell culture temperature (mosquito cells: 28 °C; mammalian cells: 37 °C) as the mutants exhibited no replication defect in mammalian cells grown at a sub-physiological temperature (28 °C). Similar effects were observed for infectious CHIKV and the closely related O'nyong-nyong virus. Intriguingly, the wildtype SGR replicated more efficiently in mammalian cells at 28 °C compared to 37 °C. To explore the mechanism behind this difference, we focused on two known antiviral pathways: interferon-stimulated genes (ISGs) and stress granules (SG). SGR replication correlated strongly with increased expression of ISGs at 37°C, but only weakly correlated at 28 °C. We also observed enhanced recruitment of SG proteins (G3BP, eIF4G, and TIA-1) into cytoplasmic sites of genome replication at 28 °C. These findings may have real-world implications as when a mosquito bites a mammal, the virus first infects cells in peripheral tissues which are often at sub-physiological temperatures. We propose that alphaviruses such as CHIKV have evolved mechanisms to both promote viral genome replication and concomitantly limit antiviral responses in these cells.
2025-04-10 | GSE264494 | GEO
Project description:Previous evaluation by different molecular and physiological assays of Staphylococcus aureus (S. aureus) responses to heat shock exposure yielded a still fragmentary view of the mechanisms determining bacterial survival or death at supra-physiological temperatures. This study analyzed diverse facets of S. aureus heat-shock adjustment by recording global transcriptomic and metabolic responses of bacterial cultures shifted for 10 min from 37oC to a sub-lethal (43oC) or eventually lethal (48oC) temperature. A relevant metabolic model of the combined action of specific stress response mechanisms with more general, energy-regulating metabolic pathways in heat-shocked S. aureus was designed. While S. aureus cultures shifted to 43oC or left at 37oC showed marginal differences in growth and survival rates, bacterial cultures exposed to 48oC showed a rapid growth arrest followed by a subsequent decline in viable counts. The most substantial heat shock-induced changes at both 43oC and 48oC occurred in transcript levels of HrcA- and CtsR-regulated genes, encoding classical chaperones DnaK and GroESL, and some Hsp100/Clp ATPases components, respectively. Other metabolic pathways up-regulated by S. aureus exposure at 48oC included genes encoding several enzymes coping with oxidative stress, and DNA damage, or/and impaired osmotic balance. Some major components of the pentose phosphate cycle and gluconeogenesis were also up-regulated, which reflected depletion of free glucose by bacterial cultures grown in Mueller-Hinton broth prior to heat shock. In contrast, most purine- and pyrimidine-synthesis pathway components and amino acyl-tRNA synthetases were down-regulated at 48oC, as well as arginine deiminase and major fermentative pathway components, such as alcohol, lactate and formate dehydrogenases. Despite the heat-induced, increased requirements for ATP-dependent macromolecular repair mechanisms combined with declining energy sources, intracellular ATP levels remained remarkably constant during heat shock. In conclusion, the sequential loss of replication and viability at 48oC cannot be explained by significant reductions in intracellular ATP levels, but may reflect ATP rerouting for macromolecular repair mechanisms and cell survival. Our metabolic model also suggests that heat-stressed S. aureus should down-regulate the production of potential, DNA-damaging reactive oxygen species that might result from electron transport-generated ATP, involving excessive levels of free heavy metals, in particular iron. Keywords: Staphylococcus aureus; heat shock; stress responses; transcriptomic profiling; physiological adjustment Comparative transcriptomic profiling of late log phase cultures of S. aureus ISP794, exposed to 43°C vs. 37°C, or 48°C vs. 37°C. We performed triplicate measurements from independently grown cultures for each heat stress condition.
2010-06-19 | E-GEOD-12920 | biostudies-arrayexpress
Project description:In this study, we aim to identify common host genes involved in pathogenesis of different Chikungunya virus strains as an attempt to recognize probable antiviral targets. We have compared the host gene regulation after infection of monkey kidney cell line (Vero) with two different wild type CHIKV strains i.e. S 27 (human, ECSA), and DRDE-06 (human, ECSA). Vero cells were mock infected or infected with two Chikungunya virus strains (S 27 and DRDE-06) and harvested at 8hpi and 18hpi. The total RNA was extracted and microarray was done using Agilent protocol.
2021-10-28 | E-MTAB-6645 | biostudies-arrayexpress
Project description:Alphavirus chikungunya Raw sequence reads
| PRJNA1314437 | ENA
Project description:Previous evaluation by different molecular and physiological assays of Staphylococcus aureus (S. aureus) responses to heat shock exposure yielded a still fragmentary view of the mechanisms determining bacterial survival or death at supra-physiological temperatures. This study analyzed diverse facets of S. aureus heat-shock adjustment by recording global transcriptomic and metabolic responses of bacterial cultures shifted for 10 min from 37oC to a sub-lethal (43oC) or eventually lethal (48oC) temperature. A relevant metabolic model of the combined action of specific stress response mechanisms with more general, energy-regulating metabolic pathways in heat-shocked S. aureus was designed. While S. aureus cultures shifted to 43oC or left at 37oC showed marginal differences in growth and survival rates, bacterial cultures exposed to 48oC showed a rapid growth arrest followed by a subsequent decline in viable counts. The most substantial heat shock-induced changes at both 43oC and 48oC occurred in transcript levels of HrcA- and CtsR-regulated genes, encoding classical chaperones DnaK and GroESL, and some Hsp100/Clp ATPases components, respectively. Other metabolic pathways up-regulated by S. aureus exposure at 48oC included genes encoding several enzymes coping with oxidative stress, and DNA damage, or/and impaired osmotic balance. Some major components of the pentose phosphate cycle and gluconeogenesis were also up-regulated, which reflected depletion of free glucose by bacterial cultures grown in Mueller-Hinton broth prior to heat shock. In contrast, most purine- and pyrimidine-synthesis pathway components and amino acyl-tRNA synthetases were down-regulated at 48oC, as well as arginine deiminase and major fermentative pathway components, such as alcohol, lactate and formate dehydrogenases. Despite the heat-induced, increased requirements for ATP-dependent macromolecular repair mechanisms combined with declining energy sources, intracellular ATP levels remained remarkably constant during heat shock. In conclusion, the sequential loss of replication and viability at 48oC cannot be explained by significant reductions in intracellular ATP levels, but may reflect ATP rerouting for macromolecular repair mechanisms and cell survival. Our metabolic model also suggests that heat-stressed S. aureus should down-regulate the production of potential, DNA-damaging reactive oxygen species that might result from electron transport-generated ATP, involving excessive levels of free heavy metals, in particular iron. Keywords: Staphylococcus aureus; heat shock; stress responses; transcriptomic profiling; physiological adjustment
2009-04-22 | GSE12920 | GEO
Project description:During cold acclimation plants increase their freezing tolerance in response to low non-freezing temperatures. This is accompanied by many physiological, biochemical and molecular changes that have been extensively investigated. In addition, many cold acclimated plants become more freezing tolerant during exposure to mild, non-damaging sub-zero temperatures. There is hardly any information available about the molecular basis of this adaptation. However, Arabidopsis thaliana is among the species that acclimate to sub-zero temperatures. This makes it possible to use the molecular and genetic tools available in this species to identify components of sub-zero signal transduction and acclimation. Here, we have used microarrays and a qRT-PCR primer platform covering 1880 genes encoding transcription factors to monitor changes in gene expression in the accessions Columbia-0, Rschew and Tenela during the first three days of sub-zero acclimation at -3°C. The results indicate that gene expression during sub-zero acclimation follows a tighly controlled time-course. Especially AP2/EREBP and WRKY transcription factors may be important regulators of sub-zero acclimation, although the CBF signal transduction pathway seems to be less important during sub-zero than during cold acclimation. Globally, we estimate that approximately 5% of all Arabidopsis genes are regulated during sub-zero acclimation. Particularly photosynthesis-related genes were down-regulated and genes belonging to the functional classes of cell wall biosynthesis, hormone metabolism and RNA regulation of transcription were up-regulated. Collectively, these data provide the first global analysis of gene expression during sub-zero acclimation and allow the identification of candidate genes for forward and reverse genetic studies into the molecular mechanisms of sub-zero acclimation. We used whole genome microarrays to monitor changes in gene expression in the Arabidopsis thaliana accessions Columbia-0, Rschew and Tenela during three days of acclimation to sub-zero temperature at -3°C after cold acclimation
2014-03-12 | GSE55835 | GEO
Project description:chikungunya virus Puerto Rico-S6 metagenome
| PRJNA281533 | ENA
Project description:A number of inhibitors of chemokine CCL2 and its receptor CCR2 are in development and may find application for treating a range of inflammatory conditions, including autoimmune and viral arthritides. Herein we sought to determine the effect of CCR2 deficiency on arthritis caused by an arthritogenic alphavirus, Chikungunya virus. Chikungunya virus (LR2006-OPY1) was injected subcutaneously into the hind foot of either CCR2 knockout or wild-type control mice (n=4-6). At day 0 and d7 post infection, RNA from the feet was harvested, the RNA was pooled (4-6 feet per time point per mouse strain) and gene expression analysis was performed using Mouse Gene ST arrays (Affymetrix).
2014-04-23 | E-GEOD-56965 | biostudies-arrayexpress