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Confocal Imaging of Double-Stranded RNA and Pattern Recognition Receptors in Negative-Sense RNA Virus Infection
Published on: January 26, 2019
Analysis of the long noncoding RNA profiles of RD and SH-SY5Y cells infected with coxsackievirus B5, using RNA
Peiying Teng1, Heng Yang2, Jing Li1
1Medical School, Kunming University of Science and Technology, No. 727, Southern Jingming Road, Chenggong District, Kunming, 650500, Yunnan, People's Republic of China.
Insights
Long noncoding RNAs (lncRNAs) are key in Coxsackievirus B5 (CV-B5) infections. This study identified lncRNAs in infected cells, revealing lncRNA-IL12A inhibits viral replication, offering new treatment targets.
Area of Science:
- Virology
- Molecular Biology
- Genomics
Background:
- Hand, foot, and mouth disease (HFMD) caused by Coxsackievirus B5 (CV-B5) poses a significant neurological risk to infants.
- Long noncoding RNAs (lncRNAs) are recognized for their crucial roles in virus-host interactions.
- The specific involvement of lncRNAs in CV-B5 pathogenesis remains largely unexplored.
Purpose of the Study:
- To investigate the expression profiles of lncRNAs in human cells infected with CV-B5.
- To identify differentially expressed lncRNAs and their potential functions in CV-B5 infection.
- To explore the therapeutic potential of lncRNAs in managing CV-B5-related diseases.
Main Methods:
- RNA sequencing was employed to profile lncRNA expression in CV-B5-infected human rhabdomyosarcoma (RD) and SH-SY5Y cells.
- Bioinformatic analyses, including Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis, were performed.
- Reverse transcription quantitative polymerase chain reaction (RT-qPCR) was used to validate the expression of selected lncRNAs.
Main Results:
- Significant numbers of upregulated and downregulated lncRNAs were identified in both RD (508 up, 760 down) and SH-SY5Y (792 up, 811 down) cells.
- The majority of differentially expressed lncRNAs were long noncoding intergenic RNAs (lincRNAs) and antisense lncRNAs.
- Pathway analysis indicated associations with disease in RD cells and involvement in signaling pathways in SH-SY5Y cells.
- lncRNA-IL12A was identified as a key player that inhibits CV-B5 replication.
Conclusions:
- lncRNAs exhibit distinct expression patterns in response to CV-B5 infection in different cell types.
- lncRNAs represent promising molecular targets for the development of novel therapeutic strategies against CV-B5 infection.
- lncRNAs may serve as potential biomarkers for distinguishing neurogenic complications associated with CV-B5 infection.
Abstract:
Hand, foot, and mouth disease caused by coxsackievirus B5 (CV-B5) is a considerable threat to infant health, especially with regard to neurological damage. Long noncoding RNAs (lncRNAs) are known to play pivotal roles in virus-host interactions. However, the roles of lncRNAs in CV-B5-host interactions have not yet been elucidated. In the current study, we used RNA sequencing to determine the expression profiles of lncRNAs in CV-B5-infected human rhabdomyosarcoma (RD) and SH-SY5Y cells. Our results showed that, of the differentially expressed lncRNAs, 508 were upregulated and 760 were downregulated in RD cells. Of these, 46.2% were long noncoding intergenic RNAs (lincRNAs), 28.6% were antisense lncRNAs, 24.1% were sense overlapping lncRNAs, and 1.0% were sense intronic lncRNAs. Moreover, 792 lncRNAs were upregulated and 811 lncRNAs were downregulated in SH-SY5Y cells, 48.6% of which were lincRNAs, 34.7% were antisense lncRNAs, 16.0% were sense overlapping lncRNAs, and 0.8% were sense intronic lncRNAs. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis showed that lncRNAs that were differentially expressed in CV-B5-infected RD cells were associated with disease, and those differentially expressed in SH-SY5Y cells were involved in signaling pathways. RT-qPCR analysis of seven lncRNAs supported these results. Moreover, our study revealed that lncRNA-IL12A inhibits viral replication. We conclude that lncRNAs constitute potential novel molecular targets for the prevention and treatment of CV-B5 infection and also may serve to distinguish neurogenic diseases caused by CV-B5 infection.
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