Journal
INTERVIROLOGY
Volume 64, Issue 3, Pages 147-155Publisher
KARGER
DOI: 10.1159/000515903
Keywords
Enterovirus 71; Long noncoding RNA; lncRNA-AK097647; IFN-λ 1; Viral replication
Categories
Funding
- Fundamental Research Funds for Shenzhen Science and Technology Innovation Committee [JCYJ20170818143952175]
- National Natural Sciences Foundation of China [52073022, 81371790, 81641093, 81371422, 81571481, 31170154]
- Major AIDS and Viral Hepatitis and Other Major Infectious Disease Prevention and Control project of China [2014ZX10001003]
- Funds for Creative Research Groups of Hubei Natural Science Foundation [2017CFA017]
- Fundamental Research Funds for the Central Universities of China
- Translational Medical Research Fund of Wuhan University School of Medicine
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The novel long noncoding RNA lncRNA-AK097647 plays a critical role in EV71 infection, with increased expression levels inhibiting the IFN-mediated host antiviral response and promoting virus replication, while knockdown of lncRNA-AK097647 significantly increases the expression of IFN and suppresses EV71 replication. Additionally, lncRNA-AK097647 was found to inhibit the phosphorylation of NF-kappa B, providing insights into a new mechanism by which EV71 evades host antiviral responses.
Background: Enterovirus 71 (EV71) infects millions of children every year in China and has become a challenge to public health. However, there is no effective treatment for EV71 infection. Long noncoding RNAs (lncRNAs) have been found to play various roles in virus replication and infection. Objective: We aimed to explore the role of a novel long noncoding RNA AK097647 (lncRNA-AK097647) during EV71 infection. Methods: To assess the role of lncRNA-AK097647 during EV71 infection, siRNAs were used to silence lncRNA-K097647 expression. RT-qPCR assay and Western blotting were applied to measure the mRNA and protein levels of EV71 VP1 and the phosphorylation of NF-kappa B. ELISA was used to detect the level of IFN-lambda 1 expression. Results: The novel lncRNA-AK097647 was upregulated in human rhabdomyosarcoma cells and the blood of hand, foot, and mouth disease patients infected with EV71, as demonstrated by RT-qPCR. Interestingly, RNAi-mediated knockdown of lncRNA-AK097647 dramatically increased the level of IFN-lambda 1 expression, resulting in the suppression of EV71 replication. In contrast, overexpression of lncRNA-AK097647 decreased the level of IFN-lambda 1 expression and resulted in increased EV71 replication. In addition, we found that lncRNA-AK097647 could inhibit the phosphorylation of NF-kappa B. Conclusion: These results suggest a novel mechanism by which EV71 evades the IFN-mediated host antiviral response by increasing lncRNA-AK097647 expression.
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