The roles of lncRNAs in the infection of enteroviruses have been barely demonstrated. In this study, we used coxsackievirus B3 (CVB3), a typical enterovirus, as a model to investigate the expression profiles and functional roles of lncRNAs in enterovirus infection. We profiled lncRNAs and mRNA expression in CVB3-infected HeLa cells by lncRNA-mRNA integrated microarrays. As a result, 700 differentially expressed lncRNAs (431 up-regulated and 269 down-regulated) and 665 differentially expressed mRNAs (299 up-regulated and 366 down-regulated) were identified in CVB3 infection. Then we performed lncRNA-mRNA integrated pathway analysis to identify potential functional impacts of the differentially expressed mRNAs, in which lncRNA-mRNA correlation network was built. According to lncRNA-mRNA correlation, we found that XLOC-001188, an lncRNA down-regulated in CVB3 infection, was negatively correlated with NFAT5 mRNA, an anti-CVB3 gene reported previously. This interaction was supported by qPCR detection following siRNA-mediated knockdown of XLOC-001188, which showed an increase of NFAT5 mRNA and a reduction of CVB3 genomic RNA. In addition, we observed that four most significantly altered lncRNAs, SNHG11, RP11-145F16.2, RP11-1023L17.1 and RP11-1021N1.2 share several common correlated genes critical for CVB3 infection, such as BRE and IRF2BP1. In all, our studies reveal the alteration of lncRNA expression in CVB3 infection and its potential influence on CVB3 replication, providing useful information for future studies of enterovirus infection.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6889111 | PMC |
| http://dx.doi.org/10.1007/s12250-019-00152-x | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Mitochondrial injury and complement dysregulation are drivers of pathological inflammation in viral myocarditis.
J Virol
January 2025
Centre for Heart Lung Innovation, St. Paul's Hospital, Vancouver, British Columbia, Canada.
Unlabelled: Enteroviruses cause nearly 1 billion global infections annually and are associated with a diverse array of human illnesses. Among these, myocarditis and the resulting chronic inflammation have been recognized as major contributing factors to virus-induced heart failure. Despite our growing understanding, very limited therapeutic strategies have been developed to address the pathological consequences of virus-induced chronic innate immune activation.
View Article and Find Full Text PDFOptimized Directed Virus Evolution to Accelerate the Generation of Oncolytic Coxsackievirus B3 Adapted to Resistant Colorectal Cancer Cells.
Viruses
December 2024
Department of Applied Biochemistry, Institute of Biotechnology, Technische Universität Berlin, 13355 Berlin, Germany.
Recently, we demonstrated that the oncolytic Coxsackievirus B3 (CVB3) strain PD-H can be efficiently adapted to resistant colorectal cancer cells through dose-dependent passaging in colorectal cancer cells. However, the method is time-consuming, which limits its clinical applicability. Here, we investigated whether the manufacturing time of the adapted virus can be reduced by replacing the dose-based passaging with volume-based passaging.
View Article and Find Full Text PDFDHX15 and Rig-I Coordinate Apoptosis and Innate Immune Signaling by Antiviral RNase L.
Viruses
December 2024
Department of Biological Sciences, University of Toledo, 2801 West Bancroft Street, Toledo, OH 43606, USA.
During virus infection, the activation of the antiviral endoribonuclease, ribonuclease L (RNase L), by a unique ligand 2'-5'-oilgoadenylate (2-5A) causes the cleavage of single-stranded viral and cellular RNA targets, restricting protein synthesis, activating stress response pathways, and promoting cell death to establish broad antiviral effects. The immunostimulatory dsRNA cleavage products of RNase L activity (RL RNAs) recruit diverse dsRNA sensors to activate signaling pathways to amplify interferon (IFN) production and activate inflammasome, but the sensors that promote cell death are not known. In this study, we found that DEAH-box polypeptide 15 (DHX15) and retinoic acid-inducible gene I (Rig-I) are essential for apoptosis induced by RL RNAs and require mitochondrial antiviral signaling (MAVS), c-Jun amino terminal kinase (JNK), and p38 mitogen-activated protein kinase (p38 MAPK) for caspase-3-mediated intrinsic apoptosis.
View Article and Find Full Text PDFSex differences in mitochondrial gene expression during viral myocarditis.
Biol Sex Differ
December 2024
Department of Cardiovascular Medicine, Mayo Clinic, Jacksonville, FL, USA.
Background: Myocarditis is an inflammation of the heart muscle most often caused by viral infections. Sex differences in the immune response during myocarditis have been well described but upstream mechanisms in the heart that might influence sex differences in disease are not completely understood.
Methods: Male and female BALB/c wild type mice received an intraperitoneal injection of heart-passaged coxsackievirus B3 (CVB3) or vehicle control.
Unlabelled: Coxsackievirus B3 (CVB3) is a non-enveloped picornavirus that can cause systemic inflammatory diseases including myocarditis, pericarditis, pancreatitis, and meningoencephalitis. We have previously reported that following infection, CVB3 localizes to mitochondria, inducing mitochondrial fission and mitophagy, while inhibiting lysosomal degradation by blocking autophagosome-lysosome fusion. This results in the release of virus-laden mitophagosomes from the host cell as infectious extracellular vesicles (EVs) which allow non-lytic viral egress.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!