Japanese Encephalitis Virus exploits the microRNA-432 to regulate the expression of Suppressor of Cytokine Signaling (SOCS) 5

Sharma, Nikhil; Kumawat, Kanhaiya Lal; Rastogi, Meghana; Basu, Anirban; Singh, Sunit K.

doi:10.1038/srep27685

Cited by 68 publications

(62 citation statements)

References 33 publications

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“…Because C19MC miRNAs attenuate viral infection in non-trophoblastic cells, [20,22,31] we sought to determine if trophoblasts might respond to viral exposure by regulating the expression of C19MC miRNAs, as has been shown in other systems [32–36]. Using three systems, we found no support for this hypothesis.…”

Section: Discussionmentioning

confidence: 90%

The expression level of C19MC miRNAs in early pregnancy and in response to viral infection

et al. 2017

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Introduction We have previously shown that miRNAs produced from the Chromosome 19 MiRNA Cluster (C19MC), which are expressed almost exclusively in primate trophoblasts and are released into the maternal circulation, reduce viral replication in non-placental cells and can modulate migratory behavior of extravillous trophoblast. We sought to define the expression pattern of C19MC miRNA in early pregnancy and in response to viral infection in vitro and in vivo. Methods We prospectively followed women undergoing in vitro fertilization (IVF) and determined their blood level of C19MC miRNA using RT-qPCR. To examine the effect of viral exposure on C19MC miRNAs expression, we used three systems: (1) a transgenic mouse overexpressing the C19MC cluster and exposed to Togaviridae during pregnancy, (2) cultured primary human trophoblasts exposed to Vesicular Stomatitis Virus in vitro, and (3) amniotic fluid from women exposed to cytomegalovirus during pregnancy. Results In 27 IVF pregnancies, C19MC miRNAs were detected as early as 2 weeks after implantation, and their levels increased thereafter. There was no change in C19MC miRNA expression levels in the mouse placenta in response to viral exposure. Similarly, Vesicular Stomatitis Virus infection of primary human trophoblast did not selectively increase C19MC miRNA expression. C19MC miRNA expression in the amniotic fluid was not affected by vertical transmission of cytomegalovirus. Discussion The expression of C19MC miRNAs in maternal circulation very early in pregnancy suggests a role in the establishment of the maternal-fetal interface. The levels of C19MC miRNA are not influenced by diverse types of viral infection.

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Section: Discussionmentioning

confidence: 90%

The expression level of C19MC miRNAs in early pregnancy and in response to viral infection

et al. 2017

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“…The growing number of reports have shown the dysregulation of microRNAs in various diseased conditions . We and others have reported the role of microRNA during JE neuroinflammation, where the virus impairs the function of microRNA and affect the down‐stream signaling in human brain microglial cells …”

Section: Discussionmentioning

confidence: 93%

“…Consequently, the previous and current study indicates that these microRNAs might be relevant to JEV infection in human microglial cells . Moreover, there are two pairs of microRNA and gene targets, which were consistent with the previous report . Nevertheless, there are several other differentially expressed microRNAs, which have not been reported earlier in case of JEV infection in microglia, and might be novel to JEV infection.…”

Section: Discussionmentioning

confidence: 99%

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Exploitation of microRNAs by Japanese Encephalitis virus in human microglial cells

Rastogi

Srivastava

Singh

2017

Journal of Medical Virology

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JEV infection in CNS leads to the JE neuroinflammation. Children and old age individual have been reported to be more prone to JEV infection. MicroRNAs are endogenous, small non-coding RNAs, which regulate the gene expression. These are ∼22 nucleotide long, conserved RNA sequence that binds at the 3'UTR of a target mRNA and regulate the post-transcriptional gene expression. The role of microRNAs has been reported in several diseases like cancer, viral infection, neuro-degeneration, diabetes etc. In the present study, the human microglial cells were infected with JEV (JaOArS982). The control and infected samples were subject to microarray profiling for microRNA expression. The microarray profile yielded differentially expressed microRNAs from JEV infected samples. The microRNA gene targets, gene ontology, annotations, and pathways were identified through various bioinformatics tools. Additionally, the pathways were mostly found common to "ubiquitin mediated proteolysis," "cytokine signaling," "maintenance of barrier function/cell junctions," JAK/STAT pathway" "Toll-like receptor signaling," "Wnt-signaling," "adhesion molecules," "apoptosis," "endocytosis," "vesicle mediated transport" etc.

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“…Human microglia, astrocytes, and brain endothelial cells are well‐documented to respond via altered cellular microRNA profile when challenged with viral proteins like HIV‐1 Tat . Another prevalent Flavivirus , Japanese encephalitis virus (JEV) is known to perturb microglial microRNA profiles upon infection . However, contribution of microRNAs in DENV‐induced neuroinflammation is poorly understood.…”

Section: Introductionmentioning

confidence: 99%

Dengue NS5 modulates expression of miR‐590 to regulate ubiquitin‐specific peptidase 42 in human microglia

2019

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Dengue virus (DENV), a member of Flaviviridae family, has become neurovirulent in humans after rapid geographical expansion. Host proteasomal machinery contains both ubiquitin ligases as well as deubiquitinases (DUBs), known to influence key cellular and biological functions. MicroRNA‐mediated modulations of DUBs in case of DENV infections have not been explored yet. DENV propagation, MiRNA overexpression, miRNA knockdown, transfection, RT‐PCR, luciferase assay, and western blotting have been used in this study to establish the interaction of miR‐590 and USP42. DENV infection in human microglial cells resulted in downregulation of host DUB‐USP42 in a dose‐dependent manner and DENV‐NS5 gene alone was found to be sufficient for this downregulation. miR‐590 was upregulated upon NS5 overexpression in a dose‐dependent manner. Downregulation of USP42 was observed with miR‐590 overexpression. The specificity of this regulation was confirmed by miR‐590 mimic and anti‐miR transfections in microglial cells. miR‐590 overexpression and knockdown affected the expression level of TRAF6 in indirect manner in microglial cells. The luciferase assay demonstrated the direct regulatory interaction between miR‐590 and 3’UTR of USP42. These findings establish that DENV‐NS5 protein can potentially modulate the host deubiquitinase protein USP42 expression via altering cellular miR‐590 levels in human microglial cells.

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Japanese Encephalitis Virus exploits the microRNA-432 to regulate the expression of Suppressor of Cytokine Signaling (SOCS) 5

Cited by 68 publications

References 33 publications

The expression level of C19MC miRNAs in early pregnancy and in response to viral infection

The expression level of C19MC miRNAs in early pregnancy and in response to viral infection

Exploitation of microRNAs by Japanese Encephalitis virus in human microglial cells

Dengue NS5 modulates expression of miR‐590 to regulate ubiquitin‐specific peptidase 42 in human microglia

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