Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptomic Analysis Initially Reveals Monocyte/Macrophage Activation Drives EV-A71-Induced Immune Dysregulation and Neural Injury in Severe HFMD

ABSTRACT: Objective Enterovirus 71 (EV-A71) is a major pathogen of severe hand, foot and mouth disease (HFMD) in children, but the mechanism by which it develops into severe HFMD remains unclear, especially the role of macrophage-mediated immune dysregulation. Methods Macrophages infected with EV-A71 were collected for transcriptomic analysis, and were indirectly co-cultured with nerve cells to observe their inhibitory effects on nerve cells. Results High concentration of EV-A71 infected macrophage supernatant inhibited SH-SY5Y cell proliferation. ENSG00000285779, TICAM2, RPL13AP26 and HNF4G are significantly different in EV-A71 or inactivated EV-A71 infected macrophages than in control. ENSG00000264324, ENSG00000260643, ISLR2, CCR7, TENM4, INO80B-WBP1, BLOC1S5-TXNDC5 are potential genes about direct virus damage or viral RNA recognition in macrophages. GO annotation and KEGG analysis indicate that EV-A71 infection cause the changes of neural receptor-ligand binding pathway, activation of specific immunity, calcium signaling pathway, and cell aggregation. Conclusions Macrophages are activated early during EV-A71 infection, thus initiating specific immunity, which is closely related to the severe HFMD. The nerve damage pathway and calcium signaling pathway caused by EV-A71 virus infection of macrophages deserve to more attention.

ORGANISM(S): Enterovirus A71

PROVIDER: GSE304239 | GEO | 2025/09/10

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Effects of Monocyte/Macrophages on the Severity of Hand, Foot, and Mouth Disease Patients due to Enterovirus

Project description:To elucidate alterations in immune cells during enterovirus 71 (EV-A71) infection and explore potential interaction mechanisms.Single-cell sequencing technology was used to sequence peripheral blood monocytes (PBMCs) obtained from a severe hand, foot and mouth disease (HFMD) patient due to EV-A71 and a healthy control.

2024-06-20 | GSE269965 | GEO

Role of Rab11 in Enterovirus A71 (EV-A71) infection

Project description:A siRNA screening using a commercially available membrane trafficking library identified Rab11 as a pro-viral host factor in motor neuron NSC34 cell line infected with EV-A71, a major causative agent of Hand, Foot and Mouth Disease (HFMD). This project aims at deciphering the role of Rab11 during EV-A71 infection by using various molecular virology and cell biology approaches. We also identified Rab11 interacting partners during EV-A71 infection by pulldown and mass spectrometry.

2024-06-28 | PXD043870 | Pride

Transcriptome analysis induced by EV-A71 infection

Project description:In this study, we aimed to adopt the transcriptome sequencing technology to obtain the different changes of transcriptome profiles after infecting with EV-A71 in human neuroblastoma cell line SH-SY5Y. And then, through systematic bioinformatics analysis, we hope to find useful clues for the pathogenesis of HFMD.

2023-06-05 | GSE151893 | GEO

A skin organoid-based infection platform identifies an inhibitor specific for HFMD

Project description:The EV-A71 poses a serious threat to the health and lives of children. The EV-A71 can be transmitted by direct and indirect skin contact. Therefore, there is an urgent need to create novel skin models using human-derived cells to study the biology and pathogenesis of the virus and facilitate drug screening. Here, we used human pluripotent stem cells-derived skin organoids (hiPSC-SOs) as a model for EV-A71 infection and found that multiple cell types within the skin organoids, including epidermal cells, hair follicle cells, fibroblasts, and nerve cells, express EV-A71 receptors and are susceptible to EV-A71 infection. We elucidated the specific response of different cell types to EV-A71 and revealed that EV-A71 infection can degrade extracellular collagen and affect fibroblasts. We found that EV-A71 can mediate epidermal cell damage through autophagy and Integrin/Hippo-YAP/TAZ signaling pathways, thereby promoting hyperproliferation of progenitor cells. Based on this finding, we identified an autophagy-associated protein as a drug target of EV-A71 and discovered an EV-A71 replication inhibitor. Altogether, these data suggest that hiPSC-SOs can be used as an infectious disease model to study skin infectious diseases, providing a valuable resource for drug screening to identify candidate virus therapeutics.

2025-01-10 | PXD047067 |

Inhibition of viral suppressor of RNAi proteins by designer peptides protects from enteroviral infection in vivo

Project description:RNA interference (RNAi) is an antiviral immunity conserved in diverse eukaryotes including mammals, while viruses encodes viral suppressors of RNAi (VSRs) as countermeasures. However, the physiological impact of RNAi on viral infection in mammals has not been fully assessed, and it also remains unknown whether antiviral RNAi can be therapeutically exploited. Here, we show that peptides designed to target enterovirus A71 (EV-A71)-encoded protein 3A, a well-characterized VSR, triggered an effective antiviral response. These VSR-targeting peptides, particularly ER-DRI, abrogated the VSR function of 3A, which enabled EV-A71-derived siRNA production and unlocked RNAi response that potently inhibited EV-A71 infection in mammals. ER-DRI treatment elicited a strong in vivo antiviral RNAi response that protected mice against lethal EV-A71 challenge. It also potently inhibited another enterovirus, Coxsackievirus-A16, dependently of RNAi. Our findings demonstrate that antiviral RNAi does have a physiologically important impact in mammals and targeting VSRs is a promising strategy for antiviral therapies.

2021-07-31 | GSE179496 | GEO

Single-cell characterization of enterovirus infection of spinal cord organoids

Project description:The mechanisms by which enteroviruses, particularly enterovirus D-68 (EV-D68) and enterovirus A-71 (EV-A71), contribute to acute flaccid myelitis (AFM), a severe neurological condition characterized by sudden muscle weakness and paralysis, remain poorly understood. To investigate the cellular tropism and infection dynamics of these enteroviruses, we utilized human spinal cord organoids (hSCOs) derived from induced pluripotent stem cells (iPSCs). We performed single-cell RNA sequencing (scRNA-seq) to profile the cellular composition of hSCOs and identify infected cell types post-infection. We found that hSCOs exhibit a diverse cellular landscape, including neurons, astrocytes, oligodendrocyte progenitor cells (OPCs), and multipotent glial progenitor cells (mGPCs), with astrocytes predominant in earlier developmental stages and neurons more abundant in later stages. Upon infection with two EV-D68 strains (US/IL/14-18952 and US/CO/18-23089) and one EVA71 strain (Tainan/4643/1998), we observed distinct viral tropism. EV-D68-18952 showed a significant increase in infected neurons, while EV-D68-23089 exhibited higher infection rates in cycling astrocytes and OPCs. In contrast, EVA71 demonstrated a broader tropism, with a statistically significant increase in infected mGPCs, suggesting enhanced infection efficiency across multiple cell types. These findings provide novel insights into the cell-type specificity of EV-D68 and EVA71 in the spinal cord, offering a deeper understanding of potential mechanisms underlying AFM pathogenesis. Understanding the dynamics of infection at single-cell resolution will inform future therapeutic strategies aimed at mitigating the neurological impact of enteroviral infections.

2025-07-30 | GSE292051 | GEO

Enterovirus 3A protein disrupts endoplasmic reticulum homeostasis through interaction with GBF1

Project description:Enterovirus A71 (EV-A71) is a single-stranded, positive sense RNA virus causing endoplasmic reticulum stress to induce or modulate downstream signaling pathways known as the unfolded protein responses (UPR). The 3A protein of EV-A71 was identified as a major regulator of the UPR caused by infection with EV-A71. To identify the molecular pathways for the 3A protein to regulate the UPR, we performed RNA sequencing (RNA-seq) with RD cells expressing the 3A protein. Wild type or defective mutant of 3A protein that carried alanine substitutions of Ile8 or Ile10 (3A-I8A or -I10A) was expressed in the cells. The RNA-seq with cells expressing either WT or mutant 3A was performed.

2024-06-16 | GSE268418 | GEO

Transcriptome analysis induced by EV-A71 infection

Project description:Transcriptome analysis induced by EV-A71 infection

| PRJNA637599 | ENA

RNP remodeling during RNA virus replication through phosphoregulation of SR proteins revealed by metabolic labeling

Project description:Mechanisms used by positive-stranded RNA viruses to control the translation-replication switch remain largely unexplored. Using metabolic labeling coupled with quantitative proteomics analyses, we unraveled the protein composition of temporal ribonucleoprotein complexes (RNPs) isolated during early and late enterovirus A71 (EV-A71) infection. Comparing the RNP components at the eclipse and maturation phase, representing early and late infection, revealed RNP remodeling over time by exchanging nuclear with cytoplasmic proteins. Among the nuclear proteins, EV-A71 infection induced the phosphorylation and cytoplasmic re-localization of nuclear SR proteins. During early infection, phosphorylated SR proteins cofractionated with the translation machinery rather than the replication organelles. During late infection, this co-localization, as well as the EV-A71-induced phosphorylated SR proteins, was no longer detected. Inhibition of SR protein phosphorylation by the kinase inhibitors SRPKIN-1 and TG003 significantly reduced the replication of several enteroviruses. Our results demonstrate the importance of phosphoregulation of SR proteins during enterovirus replication and reveal a potential target for broad-spectrum antivirals.

2025-06-04 | PXD036890 | Pride

Pathological Features of Enterovirus 71-associated Brain and Lung Damage in Mice Based on Quantitative Proteomic Analyses

Project description:Enterovirus 71 (EV71), a member of the Enterovirus genus in the Picornaviridae family, was first recognized as a dermotrophic virus that usually cause mild, self-limiting hand-foot-and-mouth disease (HFMD). However, EV71 infection can sometimes induce a variety of severe neurological complications, pulmonary edema and even death. Here, we aimed to provide an overview of proteomics characterization of EV71-infected brain and lung tissues.

2021-09-10 | PXD023819 | Pride

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data