Transcriptional Profiling of the Immune Response to Ebola Infection
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ABSTRACT:
PROVIDER: PRJNA283829 | ENA |
REPOSITORIES: ENA
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Project description:Ebola virus is the causative agent of a severe syndrome in humans with a fatality rate that can approach 90%. During infection, the host immune response is thought to become dysregulated, but the mechanisms through which this happens are not entire understood. In this study, we use microarrays to determine the host response to Ebola infection in the PBMCs of cynomolgus macaques.
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Project description:Transcriptional Profiling of the Immune Response to Marburg Infection
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Project description:The purpose of this experiment was to obtain samples for transcriptome analysis using wild-type viruses: Zaire Ebola (ZEBOV '76) and Reston Ebola (REBOV '08). Overview of Experiment: Cells: Immortalized Human Hepatocytes (IHH); seed 60,000 cells per well in a 24-well plate. Infected with a multiplicity of infection (MOI) of 0.5. After infection, 3x wash with PBS and replace with 5% FCS DMEM without NaPyr or NEAA. Time matched mocks done in triplicate from same cell stock as rest of samples. Time Points = 0, 8, 24, 48, and 72 hrs post infection in triplicate. (For miRNA: 8, 24, 48, 72 hours.)
2015-02-04 | E-GEOD-65573 | biostudies-arrayexpress
Project description:The purpose of this experiment was to obtain samples for mRNA analysis in IHH cells infected with Zaire Ebola virus and mutants: Zaire Ebola virus: This wild-type Ebola virus - strain Mayinga - was isolated from a fatal human case in Zaire (now known as the Democratic Republic of Congo) in 1976 Zaire Ebola virus, VP35 R312A possesses a R312A mutation in the VP35 protein. Zaire Ebola virus, delta sGP. Lacks the ability to produce non-structural protein, the secreted glycoprotein (sGP). Zaire Ebola virus, delta mucin. Lacks the mucin-like domain (MLD), which contains both N-linked and O-linked glycosylation sites, for the glycoproteins. Overview of Experiment: Cells: Immortalized Human Hepatocytes (IHH); seed 60,000 cells per well in a 24-well plate. Infected with a multiplicity of infection (MOI) of 0.5. After infection, 3x wash with PBS and replace with 5% FCS DMEM without NaPyr or NEAA. Time matched mocks done in triplicate from same cell stock as rest of samples. Time Points = 0, 6, 12, 24, 48, and 72 hrs post infection in triplicate.
2015-06-18 | E-GEOD-69943 | biostudies-arrayexpress
Project description:The purpose of this experiment was to obtain samples for mRNA analysis in IHH cells infected with Zaire Ebola virus and mutants: Zaire Ebola virus: This wild-type Ebola virus - strain Mayinga - was isolated from a fatal human case in Zaire (now known as the Democratic Republic of Congo) in 1976 Zaire Ebola virus, VP35 R312A possesses a R312A mutation in the VP35 protein. Zaire Ebola virus, delta sGP. Lacks the ability to produce non-structural protein, the secreted glycoprotein (sGP). Zaire Ebola virus, delta mucin. Lacks the mucin-like domain (MLD), which contains both N-linked and O-linked glycosylation sites, for the glycoproteins. Overview of Experiment: Cells: Immortalized Human Hepatocytes (IHH); seed 60,000 cells per well in a 24-well plate. Infected with a multiplicity of infection (MOI) of 0.5. After infection, 3x wash with PBS and replace with 5% FCS DMEM without NaPyr or NEAA. Time matched mocks done in triplicate from same cell stock as rest of samples. Time Points = 0, 6, 12, 24, 48, and 72 hrs post infection in triplicate.
2015-06-18 | E-GEOD-69942 | biostudies-arrayexpress
Project description:Ebola virus can cause a severe and often fatal hemorrhagic fever in humans and other mammals, known as Ebola virus disease (EVD),the mechanism of how this pathogenesis comes about is not well understood, but it is well accepted that pathogenesis is significantly driven by a hyperactive immune response. To better understand the overall response to Ebola virus challenge, we undertook a transcriptomic analysis using the whole blood of EBOV infection patients.
2023-12-31 | GSE83563 | GEO
Project description:Ebola virus (EBOV) causes epidemics with high mortality, yet remains understudied due to the challenge of experimentation in high-containment and outbreak settings. Here, we used single-cell transcriptomics and CyTOF-based single-cell protein quantification to characterize peripheral immune cells during EBOV infection in rhesus monkeys. We obtained 100,000 transcriptomes and 15,000,000 protein profiles, providing insight into pathogenesis: e.g., immature, proliferative monocyte-lineage cells with reduced antigen presentation capacity replace conventional monocyte subsets, while lymphocytes upregulate apoptosis genes and decline in abundance. By quantifying intracellular viral RNA, we identify molecular determinants of tropism among circulating immune cells and examine temporal dynamics in viral and host gene expression. Within infected cells, EBOV down-regulates STAT1 mRNA and interferon signaling, and up-regulates putative pro-viral genes (e.g., DYNLL1 and HSPA5), nominating pathways the virus manipulates for its replication. This study sheds light on EBOV tropism, replication dynamics, and elicited immune response, and provides a framework for characterizing host-virus interactions under maximum containment.
2020-09-23 | GSE158390 | GEO
Project description:Long non-coding RNAs (lncRNAs) are pivotal mediators of systemic immune response to viral infection yet most studies concerning their expression and functions upon immune stimulation are limited to in vitro bulk cell populations. This strongly constrains our understanding of how lncRNA expression varies at single-cell resolution, and whether differences with protein coding genes exist in their cell-type specific immune regulatory roles. Here, we perform the first in-depth characterization of lncRNA expression variation at single-cell resolution during Ebola virus (EBOV) infection in vivo. Using bulk RNA-sequencing from 119 samples and 12 tissue types, we significantly expand the current macaque lncRNA annotation. We then profile lncRNA expression variation in immune circulating single-cells during EBOV infection and find that lncRNAs’ expression in fewer cells is a major differentiating factor to their protein coding gene counterparts. Upon EBOV infection, lncRNAs present dynamic and mostly cell-type specific changes in their expression profiles especially in monocytes, the main cell type targeted by EBOV. Such changes are associated with gene regulatory modules related to important innate immune responses such as interferon response and purine metabolism. Within infected cells, several lncRNAs have correlated and anti-correlated expression with viral load, suggesting that expression of some of these lncRNAs might be directly hijacked by EBOV to attack host cells. This study provides novel insights on the roles that lncRNAs play in the host response to acute viral infection and paves the way for future lncRNA studies at single-cell resolution.
2023-04-26 | GSE191315 | GEO
Project description:Long non-coding RNAs (lncRNAs) are pivotal mediators of systemic immune response to viral infection yet most studies concerning their expression and functions upon immune stimulation are limited to in vitro bulk cell populations. This strongly constrains our understanding of how lncRNA expression varies at single-cell resolution, and whether differences with protein coding genes exist in their cell-type specific immune regulatory roles. Here, we perform the first in-depth characterization of lncRNA expression variation at single-cell resolution during Ebola virus (EBOV) infection in vivo. Using bulk RNA-sequencing from 119 samples and 12 tissue types, we significantly expand the current macaque lncRNA annotation. We then profile lncRNA expression variation in immune circulating single-cells during EBOV infection and find that lncRNAs’ expression in fewer cells is a major differentiating factor to their protein coding gene counterparts. Upon EBOV infection, lncRNAs present dynamic and mostly cell-type specific changes in their expression profiles especially in monocytes, the main cell type targeted by EBOV. Such changes are associated with gene regulatory modules related to important innate immune responses such as interferon response and purine metabolism. Within infected cells, several lncRNAs have correlated and anti-correlated expression with viral load, suggesting that expression of some of these lncRNAs might be directly hijacked by EBOV to attack host cells. This study provides novel insights on the roles that lncRNAs play in the host response to acute viral infection and paves the way for future lncRNA studies at single-cell resolution.
2023-04-26 | GSE191102 | GEO