Changes in cellular gene expression during prototype foamy virus infection
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PROVIDER: PRJNA823659 | ENA |
REPOSITORIES: ENA
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Project description:Changes in cellular gene expression levels in the presence of prototype foamy virus (PFV) infection were analyzed using a transcriptomic sequencing system. The results showed that the greatest changes in cellular gene expression levels were observed after 24h of infection compared to 6h and 12h of PFV infection. These results provide a reference for our study of PFV and host interactions.
2022-04-08 | GSE200199 | GEO
Project description:While numerous viral microRNAs (miRNAs) expressed by DNA viruses, especially herpesvirus family members, have been reported, there have been very few reports of miRNAs derived from RNA viruses. Here we describe three miRNAs expressed by bovine foamy virus (BFV), a member of the spumavirus subfamily of retroviruses, in both BFV-infected cultured cells and BFV-infected cattle. All three viral miRNAs are initially expressed in the form of an ∼ 122-nucleotide (nt) pri-miRNA, encoded within the BFV long terminal repeat U3 region, that is subsequently cleaved to generate two pre-miRNAs that are then processed to yield three distinct, biologically active miRNAs. The BFV pri-miRNA is transcribed by RNA polymerase III, and the three resultant mature miRNAs were found to contribute a remarkable ∼ 70% of all miRNAs expressed in BFV-infected cells. These data document the second example of a retrovirus that is able to express viral miRNAs by using embedded proviral RNA polymerase III promoters. Small RNA profiling of Bovine Foamy Virus (BFV)-infected cells through total small RNA deep sequencing
2015-04-07 | E-GEOD-67620 | biostudies-arrayexpress
Project description:BackgroundFoamy viruses (FVs) are retroviruses with unique replication strategies that cause lifelong latent infections in their hosts. FVs can also produce foam-like cytopathic effects in vitro. However, the effect of host cytokines on FV replication requires further investigation. Although interferon induced transmembrane (IFITMs) proteins have become the focus of antiviral immune response research due to their broad-spectrum antiviral ability, it remains unclear whether IFITMs can affect FV replication.MethodIn this study, the PFV virus titer was characterized by measuring luciferase activity after co-incubation of PFVL cell lines with the cell culture supernatants (cell-free PFV) or the cells transfected with pcPFV plasmid/infected with PFV (cell-associated PFV). The foam-like cytopathic effects of PFV infected cells was observed to reflect the virus replication. The total RNA of PFV infected cells was extracted, and the viral genome was quantified by Quantitative reverse transcription PCR to detect the PFV entry into target cells.ResultsIn the present study, we demonstrated that IFITM1-3 overexpression inhibited prototype foamy virus (PFV) replication. In addition, an IFITM3 knockdown by small interfering RNA increased PFV replication. We further demonstrated that IFITM3 inhibited PFV entry into host cells. Moreover, IFITM3 also reduced the number of PFV envelope proteins, which was related to IFITM3 promoted envelope degradation through the lysosomal pathway.ConclusionsTaken together, these results demonstrate that IFITM3 inhibits PFV replication by inhibiting PFV entry into target cells and reducing the number of PFV envelope.
| S-EPMC9682733 | biostudies-literature
Project description:Macrophages in atherosclerotic aorta are major population in lesion and contributes to lesion formation by becoming foam cells. To investigate in vivo transcriptome profiles of those macrophages, we extracted foamy and non-foamy macrophages from atherosclerotic aorta using lipid probe-based flow cytometry sorting. Our data indicates that intima non-foamy and foamy macrophages show different mRNA expressions. Rather than non-foamy macrophages, foamy macrophages expressed more genes related to cholesterol metabolism, oxidative phosphorylation, lysosome and so on. The non-foamy macrophages expressed more genes related to immune response (Il-1b related pathways, TNF, TLR signaling pathways) than foamy macrophages.
2018-08-30 | GSE116239 | GEO
Project description:After spinal cord injury (SCI), infiltrating macrophages undergo excessive phagocytosis of myelin and cellular debris, forming lipid-laden foamy macrophages. To understand their role in the cellular pathology of SCI, investigation of foamy macrophage phenotype in vitro revealed a unique inflammatory profile, increased reactive oxygen species (ROS) production, and mitochondrialdysfunction. Bioinformatic analysis identified PI3K as a regulator of inflammation in foamy macrophages, and pharmacological inhibition of this pathway decreased lipid content and inflammatory cytokine and ROS production in these cells. Macrophage-specific inhibition of PI3K using liposomes significantly decreased foamy macrophages at the injury site after a mid-thoracic contusive SCI in mice. RNA sequencing and in vitro analysis of foamy macrophages revealed increased autophagy after PI3K inhibition as a potential mechanism for reduced cellular lipid accumulation. Together, our data suggest that formation of pro-inflammatory foamy macrophages after SCI is due to activation of PI3K signaling that leads to decreased autophagy.
2023-12-05 | GSE237511 | GEO
Project description:Atherosclerosis-associated vascular disease is the leading cause of death worldwide. Clinical and experimental data demonstrated that circulating monocytes internalize plasma lipoproteins and become lipid-laden foamy cells in hypercholesterolemic subjects. This study was designed to identify the endocytic mechanisms responsible for foamy monocyte formation, perform functional and transcriptomic analysis of foamy and non-foamy monocytes, and characterize specific monocyte subsets in the circulation from normocholesterolemic controls and hypercholesterolemic patients. The presence of foamy monocytes was confirmed in hypercholesterolemic mice and humans via flow cytometry analysis. High resolution scanning electron microscopy (SEM) and quantification of FITC/TRITC-dextran internalization demonstrated macropinocytosis stimulation in human (THP-1) and wild type murine monocytes in vitro. Stimulation of macropinocytosis induced foamy monocyte formation in the presence of unmodified, native LDL (nLDL) and oxidized LDL (ox-LDL) in vitro. Genetic blockade of macropinocytosis (LysMCre+ Nhe1f/f) inhibited foamy monocyte formation in hypercholesterolemic mice in vivo and attenuated monocyte adhesion to atherosclerotic aortas ex vivo. qRT-PCR quantified mRNA levels of major scavenger receptors (SR) in foamy and non-foamy monocytes and identified CD36 as a major SR increasing in response to lipid loading. Deletion of CD36 (Cd36-/-) inhibited foamy monocyte formation in hypercholesterolemic mice. Mechanistic studies identified NADPH oxidase 2 (Nox2)-derived superoxide (O2⋅−) as an important downstream signaling molecule stimulating macropinocytosis in monocytes. Bulk RNA-sequencing characterized transcriptional differences between non-foamy and foamy monocytes and macrophages. Flow cytometry analysis of CD14 and CD16 expression demonstrated a significant increase in intermediate monocytes in hypercholesterolemic patients compared to normocholesterolemic controls. These results provide novel insights into the mechanisms of foamy monocyte formation and potentially identify new therapeutic targets in the treatment of atherosclerosis.
2024-12-26 | GSE278101 | GEO
Project description:The general aim of this paper is to explore a little further into molecular biology of the interaction between virus and host cell. We seek to use cDNA microarray technology, one revolutionary methodological advance, to perform a high throughput analysis of cDNA clones with the intent of identifying genes expressed in association with the infection with BKV in Vero cells (green monkey kidney cells). This technology, which can supply quantitative expression information for many thousands of genes simultaneously, has been used to classify the cellular genes at transcript levels in different physiological states of a tissue or cell. Accordingly, in this study, we have constructed a cDNA microarray containing 32448 spots (quadruplication of 7,334 human cDNAs and doping controls) to study that BKV infection of Vero cells. Our purposes were (i) to appraise whether cDNA microarrays could be employed to investigate the expression of cellular genes during the 5 time courses (5, 10, 15, 19 and 25 days post-infection (dpi)) of infection with BKV, (ii) to identify any genes that resulted in up-regulation or down-regulation of cell gene expression transcription, (iii) to determine the etiological role of BKV in nephropathy and/or neoplasia, (iv) to form a clearer picture of virus-associated pathophysiology in kidney. Keywords: BK virus, BKV, cDNA microarray, Vero cell We used a loop design in this study. cDNA microarray experiment consisted of ten RNA samples, including BKV-infected samples and their corresponding uninfected controls in 5 different time points. See supplementary PDF file for additional information
2010-06-26 | E-GEOD-8085 | biostudies-arrayexpress
Project description:The general aim of this paper is to explore a little further into molecular biology of the interaction between virus and host cell. We seek to use cDNA microarray technology, one revolutionary methodological advance, to perform a high throughput analysis of cDNA clones with the intent of identifying genes expressed in association with the infection with BKV in Vero cells (green monkey kidney cells). This technology, which can supply quantitative expression information for many thousands of genes simultaneously, has been used to classify the cellular genes at transcript levels in different physiological states of a tissue or cell. Accordingly, in this study, we have constructed a cDNA microarray containing 32448 spots (quadruplication of 7,334 human cDNAs and doping controls) to study that BKV infection of Vero cells. Our purposes were (i) to appraise whether cDNA microarrays could be employed to investigate the expression of cellular genes during the 5 time courses (5, 10, 15, 19 and 25 days post-infection (dpi)) of infection with BKV, (ii) to identify any genes that resulted in up-regulation or down-regulation of cell gene expression transcription, (iii) to determine the etiological role of BKV in nephropathy and/or neoplasia, (iv) to form a clearer picture of virus-associated pathophysiology in kidney. Keywords: BK virus, BKV, cDNA microarray, Vero cell
2008-06-11 | GSE8085 | GEO
Project description:Lipid metabolism is an intricate yet crucial cellular process co-opted by multiple viruses for replication and biogenesis. Transmembrane Protein 41B (TMEM41B) and Vacuole Membrane Protein 1 (VMP1) are two recently identified ER-resident lipid scramblases that play a role in autophagosome formation and cellular lipid metabolism. Importantly, TMEM41B is also a newly validated host dependency factor required for productive infection of several medically important enveloped RNA viruses, such as flaviviruses and human coronaviruses. However, the exact underlying mechanism of TMEM414B in modulating viral infections remains an open question. Here, we uncovered that TMEM41B and VMP1 deficiencies severely impaired replication of flavivirus and human coronavirus via multiple parallel cellular mechanisms. In accordance with previous reports, we validated that both TMEM41B and VMP1 are indispensable for all four serotypes of dengue virus (DENV) and human coronavirus OC43 (HCoV-OC43) to infect human cells, but not chikungunya virus, an alphavirus. Impaired dengue virus replication in TMEM41B and VMP1 deficient cells could induce a robust activation of innate immune RNA sensing as evidenced by hyperactivation of RIG-I and MDA5. However, this phenomenon was a consequence but not the root cause of the diminished viral replication. Notably, the impact of TMEM41B deficiency on DENV replication could be reversed by complementing the cells using exogenous unsaturated fatty acids, indicating a metabolic role for TMEM41B in flavivirus infection. Furthermore, we found that derailed cellular energy metabolism could be a contributing factor to block DENV infection as TMEM41B and VMP1 deficient cells harbored higher levels of compromised mitochondria that exhibited aberrant functions in facilitating beta-oxidation. Using lipidome and metabolome profiling of TMEM41B and VMP1 deficient cells, we further revealed that each of these genetic deficiencies result in distinctive cellular metabolic dysregulations, underlining their necessity for a balanced metabolic landscape, and strengthening the metabolic role of these ER membrane proteins in facilitating virus infection. Our results highlighted that TMEM41B and VMP1 are required for homeostasis of cellular metabolism, and this metabolic role contributes to their essentiality in facilitating DENV infection.
2022-05-11 | ST002164 | MetabolomicsWorkbench