Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1078593 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR28026156_1.fastq.gz | Fastqsanger.gz | |||
| SRR28026156_2.fastq.gz | Fastqsanger.gz | |||
| SRR28026157_1.fastq.gz | Fastqsanger.gz | |||
| SRR28026157_2.fastq.gz | Fastqsanger.gz | |||
| SRR28026158_1.fastq.gz | Fastqsanger.gz |
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Project description:Here, we examined the transcriptional and epigenetic (DNA methylation) responses to viral infection in honey bee workers. One-day old worker honey bees were fed solutions containing Israeli Acute Paralysis Virus (IAPV), a virus which causes muscle paralysis and death and has previously been associated with colony loss. Uninfected control and infected, symptomatic bees were collected within 20-24 hours after infection. Worker fat bodies, the primary tissue involved in metabolism, detoxification and immune responses, were collected for analysis. We performed transcriptome- and bisulfite-sequencing of the worker fat bodies to identify genome-wide gene expression and DNA methylation patterns associated with viral infection. There were 753 differentially expressed genes (FDR<0.05) in infected versus control bees, including several genes involved in epigenetic and antiviral pathways. DNA methylation status of 156 genes (FDR<0.1) changed significantly as a result of the infection, including those involved in antiviral responses in humans. There was no significant overlap between the significantly differentially expressed and significantly differentially methylated genes, and indeed, the genomic characteristics of these sets of genes were quite distinct. Our results indicate that honey bees have two distinct molecular pathways, mediated by transcription and methylation, that modulate protein levels and/or function in response to viral infections. Examination of epigenomic and transcriptomic antiviral responses to Israeli Acute Paralysis Virus in honey bees
2015-02-06 | E-GEOD-65659 | biostudies-arrayexpress
Project description:Here, we examined the transcriptional and epigenetic (DNA methylation) responses to viral infection in honey bee workers. One-day old worker honey bees were fed solutions containing Israeli Acute Paralysis Virus (IAPV), a virus which causes muscle paralysis and death and has previously been associated with colony loss. Uninfected control and infected, symptomatic bees were collected within 20-24 hours after infection. Worker fat bodies, the primary tissue involved in metabolism, detoxification and immune responses, were collected for analysis. We performed transcriptome- and bisulfite-sequencing of the worker fat bodies to identify genome-wide gene expression and DNA methylation patterns associated with viral infection. There were 753 differentially expressed genes (FDR<0.05) in infected versus control bees, including several genes involved in epigenetic and antiviral pathways. DNA methylation status of 156 genes (FDR<0.1) changed significantly as a result of the infection, including those involved in antiviral responses in humans. There was no significant overlap between the significantly differentially expressed and significantly differentially methylated genes, and indeed, the genomic characteristics of these sets of genes were quite distinct. Our results indicate that honey bees have two distinct molecular pathways, mediated by transcription and methylation, that modulate protein levels and/or function in response to viral infections.
2015-02-06 | GSE65659 | GEO
Project description:There were important gaps in our knowledge of Israeli acute paralysis virus (IAPV), when IAPV was tightly linked to bee Colony Collapse Disorder (CCD), the mysterious disease that, starting in 2006-2007, has been wiping out honey bees in the US. To fill in these gaps we studied the molecular basis of transmission, pathogenesis, and genetic diversity of IAPV infection in honey bees. We investigated the impact of IAPV infection on colony losses and host transcriptional response to IAPV infections, and exploited the potential of RNAi-based strategies for treating viral diseases in honey bees. Our study clearly shows that IAPV has become established as a persistent infection and is highly prevalent in the honey bee population. The existence of both horizontal and vertical transmission pathways of the virus likely accounts for the high prevalence of IAPV in bees. While IAPV is probably not the only culprit responsible for CCD, its ability to cause increased mortality in honey bees is firmly demonstrated. The phenotypic differences in pathology among different strains of IAPV may be due to their high level of standing genetic variation. The JAK-STAT pathway, along with other signaling events such as mTOR and MAPK pathways, likely involves honey bees’ antiviral immune responses to the IAPV infection. The identification of IAPV-encoded putative suppressor of RNAi and evidence that silencing the RNAi suppressor led to a significant reduction in IAPV replication in infected bees illustrates the therapeutic potential of targeting viral suppressor protein to reduce virus replication. Our study gives direction for developing strategies to reduce colony losses due to viral diseases. Adult worker bees and brood were collected from colonies that were declining and identified with IAPV infections and its control with 6 replications per group.
2014-04-08 | E-GEOD-46278 | biostudies-arrayexpress
Project description:There were important gaps in our knowledge of Israeli acute paralysis virus (IAPV), when IAPV was tightly linked to bee Colony Collapse Disorder (CCD), the mysterious disease that, starting in 2006-2007, has been wiping out honey bees in the US. To fill in these gaps we studied the molecular basis of transmission, pathogenesis, and genetic diversity of IAPV infection in honey bees. We investigated the impact of IAPV infection on colony losses and host transcriptional response to IAPV infections, and exploited the potential of RNAi-based strategies for treating viral diseases in honey bees. Our study clearly shows that IAPV has become established as a persistent infection and is highly prevalent in the honey bee population. The existence of both horizontal and vertical transmission pathways of the virus likely accounts for the high prevalence of IAPV in bees. While IAPV is probably not the only culprit responsible for CCD, its ability to cause increased mortality in honey bees is firmly demonstrated. The phenotypic differences in pathology among different strains of IAPV may be due to their high level of standing genetic variation. The JAK-STAT pathway, along with other signaling events such as mTOR and MAPK pathways, likely involves honey bees’ antiviral immune responses to the IAPV infection. The identification of IAPV-encoded putative suppressor of RNAi and evidence that silencing the RNAi suppressor led to a significant reduction in IAPV replication in infected bees illustrates the therapeutic potential of targeting viral suppressor protein to reduce virus replication. Our study gives direction for developing strategies to reduce colony losses due to viral diseases.
2014-04-08 | GSE46278 | GEO
Project description:Cricket paralysis virus Transcriptome or Gene expression
| PRJNA248688 | ENA