miR-27a suppresses EV71 replication by directly targeting EGFR

Zhang, Lianglu; Chen, Xiong; Shi, Yingying; Zhou, Benhong; Du, Chen; Liu, Yongjuan; Han, Song; Yin, Jun; Peng, Biwen; He, Xiaohua; Liu, Wanhong

doi:10.1007/s11262-014-1114-4

Cited by 28 publications

(27 citation statements)

References 23 publications

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“…The upregulated miR-363 is also known to induce apoptosis (Zhang et al, 2014; Zhou et al, 2014; Hu et al, 2015; Li et al, 2015). The upregulation of miR-21-3p and miR-363 in PPRV infections suggests synergistic effect of these miRs along with the virus in inducing apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Modulation of Host miRNAs Transcriptome in Lung and Spleen of Peste des Petits Ruminants Virus Infected Sheep and Goats

et al. 2017

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Peste des petits ruminants (PPR) is one of the highly contagious viral disease, characterized by fever, sore mouth, conjunctivitis, gastroenteritis, and pneumonia, primarily affecting sheep and goats. Reports suggested variable host response in goats and sheep and this host response vis-a-vis the expression of microRNAs (miRNAs) has not been investigated. Here, miRNAs were sequenced and proteomics data were generated to identify the role of differentially expressed miRNA (DEmiRNA) in PPR virus (PPRV) infected lung and spleen tissues of sheep and goats. In lungs, 67 and 37 DEmiRNAs have been identified in goats and sheep, respectively. Similarly, in spleen, 50 and 56 DEmiRNAs were identified in goats and sheep, respectively. A total of 20 and 11 miRNAs were found to be common differentially expressed in both the species in PPRV infected spleen and lung, respectively. Six DEmiRNAs—miR-21-3p, miR-1246, miR-27a-5p, miR-760-3p, miR-320a, and miR-363 were selected based on their role in viral infections, apoptosis, and fold change. The target prediction analysis of these six selected DEmiRNAs from the proteome data generated, revealed involvement of more number of genes in lung and spleen of goats than in sheep. On gene ontology analysis of host target genes these DEmiRNAs were found to regulate several immune response signaling pathways. It was observed that the pathways viz. T cell receptor signaling, Rap1 signaling, Toll-like receptor signaling, and B cell receptor signaling governed by DEmiRNAs were more perturbed in goats than in sheep. The data suggests that PPRV-induced miR-21-3p, miR-320a, and miR-363 might act cooperatively to enhance viral pathogenesis in the lung and spleen of sheep by downregulating several immune response genes. The study gives an important insight into the molecular pathogenesis of PPR by identifying that the PPRV—Izatnagar/94 isolate elicits a strong host response in goats than in sheep.

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Section: Discussionmentioning

confidence: 99%

Modulation of Host miRNAs Transcriptome in Lung and Spleen of Peste des Petits Ruminants Virus Infected Sheep and Goats

et al. 2017

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“…According to current and our previous studies, rhabdomyosarcoma (RD) cells and the Henrietta Lacks strain of cancer (HeLa) cells can be used as in vitro models to investigate the interplay between EV71 and its host [16, 27–29]. To determine whether hsa-let-7c-5p is involved in EV71 infection, we first examined the expression of mature hsa-let-7c-5p in uninfected and EV71-infected RD cells by stem-loop quantitative reverse transcription polymerase chain reaction (qRT-PCR).…”

Section: Resultsmentioning

confidence: 99%

“…Previously, we have found that miR-27a expression is downregulated and that hsa-let-7c-5p expression is upregulated in RD cells during EV71 infection. Further, we have reported that miR-27a overexpression suppresses viral replication through the regulation of EGFR-mediated pathways [16]. It is of interest to investigate the role of hsa-let-7c-5p miRNA upregulation in EV71 infection.…”

Section: Discussionmentioning

confidence: 99%

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Hsa-let-7c-5p augments enterovirus 71 replication through viral subversion of cell signaling in rhabdomyosarcoma cells

Zhou

Chu

et al. 2017

Cell Biosci

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BackgroundHuman enterovirus 71 (EV71) causes severe hand, foot and mouse disease, accompanied by neurological complications. During the interaction between EV71 and the host, the virus subverts host cell machinery for its own replication. However, the roles of microRNAs (miRNAs) in this process remain obscure.ResultsIn this study, we found that the miRNA hsa-let-7c-5p was significantly upregulated in EV71-infected rhabdomyosarcoma cells. The overexpression of hsa-let-7c-5p promoted replication of the virus, and the hsa-let-7c-5p inhibitor suppressed viral replication. Furthermore, hsa-let-7c-5p targeted mitogen-activated protein kinase kinase kinase kinase 4 (MAP4K4) and inhibited its expression. Interestingly, downregulation of MAP4K4 expression led to an increase in EV71 replication. In addition, MAP4K4 knockdown or transfection with the hsa-let-7c-5p mimic led to activation of the c-Jun NH2-terminal kinase (JNK) signaling pathway, whereas the hsa-let-7c-5p inhibitor inhibited activation of this pathway. Moreover, EV71 infection promoted JNK pathway activation to facilitate viral replication.ConclusionsOur data suggested that hsa-let-7c-5p facilitated EV71 replication by inhibiting MAP4K4 expression, which might be related to subversion of the JNK pathway by the virus. These results may shed light on a novel mechanism underlying the defense of EV71 against cellular responses. In addition, these findings may facilitate the development of new antiviral strategies for use in future therapies.Electronic supplementary materialThe online version of this article (doi:10.1186/s13578-017-0135-9) contains supplementary material, which is available to authorized users.

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“…Oligonucleotides: Previous reports have described the antiviral effects of RNA-based therapeutics, such as siRNA,shRNA and miRNA, targeting the VP1, 3D, 2C genes, or the 3' UTR of the HEV71 genome, resulting in antiviral activity [121][122][123][124][125][126][127][128] . However, whilst plasmid-derived shRNAs are widely used for laboratory studies, they are not suitable for antiviral therapy.…”

Section: Interferonsmentioning

confidence: 99%

Therapeutic and prevention strategies against human enterovirus 71 infection

Kok

2015

WJV

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Human enterovirus 71 (HEV71) is the cause of hand, foot and mouth disease and associated neurological complications in children under five years of age. There has been an increase in HEV71 epidemic activity throughout the Asia-Pacific region in the past decade, and it is predicted to replace poliovirus as the extant neurotropic enterovirus of highest global public health significance. To date there is no effective antiviral treatment and no vaccine is available to prevent HEV71 infection. The increase in prevalence, virulence and geographic spread of HEV71 infection over the past decade provides increasing incentive for the development of new therapeutic and prevention strategies against this emerging viral infection. The current review focuses on the potential, advantages and disadvantages of these strategies. Since the explosion of outbreaks leading to large epidemics in China, research in natural therapeutic products has identified several groups of compounds with anti-HEV71 activities. Concurrently, the search for effective synthetic antivirals has produced promising results. Other therapeutic strategies including immunotherapy and the use of oligonucleotides have also been explored. A sound prevention strategy is crucial in order to control the spread of HEV71. To this end the ultimate goal is the rapid development, regulatory approval and widespread implementation of a safe and effective vaccine. The various forms of HEV71 vaccine designs are highlighted in this review. Given the rapid progress of research in this area, eradication of the virus is likely to be achieved. Core tip: This review focuses on therapeutic and prevention strategies for the control of human enterovirus 71 infection. Therapeutic strategies highlighted include natural products, synthetic antivirals, immunotherapy, and the use of olignucleotides. Prevention strategies such as surveillance, physical prevention, and vaccine development form the second part of the review.Kok CC. Therapeutic and prevention strategies against human enterovirus 71 infection. World J Virol 2015; 4(2): 78-95 Available from:

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miR-27a suppresses EV71 replication by directly targeting EGFR

Cited by 28 publications

References 23 publications

Modulation of Host miRNAs Transcriptome in Lung and Spleen of Peste des Petits Ruminants Virus Infected Sheep and Goats

Modulation of Host miRNAs Transcriptome in Lung and Spleen of Peste des Petits Ruminants Virus Infected Sheep and Goats

Hsa-let-7c-5p augments enterovirus 71 replication through viral subversion of cell signaling in rhabdomyosarcoma cells

Therapeutic and prevention strategies against human enterovirus 71 infection

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