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      miR-146a suppresses cellular immune response during Japanese encephalitis virus JaOArS982 strain infection in human microglial cells.

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          Abstract

          Japanese encephalitis virus (JEV) is the causative agent of Japanese encephalitis which is more prevalent in South and Southeast Asia. JEV is a neurotropic virus which infiltrates into the brain through vascular endothelial cells. JEV infects neurons and microglial cells which causes neuronal damage and inflammation. However, JEV also evades the cellular immune response to survive in host cells. Viruses are known to modulate the expression of microRNAs, which in turn modulate cellular immune response by targeting expression of antiviral genes. The aim of this study is to understand the anti-inflammatory role of miR-146a during JEV infection, which facilitates immune evasion.

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          Ecology and geographical expansion of Japanese encephalitis virus.

          Andrew van den Hurk, Scott Ritchie, John S. Mackenzie (2009)
          Japanese encephalitis virus (JEV) (Flavivirus: Flaviviridae) is a leading cause of encephalitis in eastern and southern Asia. The virus is maintained in a zoonotic cycle between ardeid wading birds and/or pigs and Culex mosquitoes. The primary mosquito vector of JEV is Culex tritaeniorhynchus, although species such as Cx. gelidus, Cx. fuscocephala, and Cx. annulirostris are important secondary or regional vectors. Control of JEV is achieved through human and/or swine vaccination, changes in animal husbandry, mosquito control, or a combination of these strategies. This review outlines the ecology of JEV and examines the recent expansion of its geographical range, before assessing its ability to emerge in new regions, using the hypothetical establishment in the United States as a case study.
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            MicroRNAs as mediators of viral evasion of the immune system.

            Bryan R. Cullen (2013)
            Cellular microRNAs serve key roles in the post-transcriptional regulation of almost every cellular gene-regulatory pathway, and it therefore is not surprising that viruses have found ways to subvert this process. Several viruses encode microRNAs that directly downregulate the expression of factors of the innate immune system, including proteins involved in promoting apoptosis and recruiting effector cells of the immune system. Viruses have also evolved the ability to downregulate or upregulate the expression of specific cellular miRNAs to enhance their replication. This Review provides an overview of the present knowledge of the complex interactions of viruses with the microRNA machinery of cells.
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              MicroRNA 146a (miR-146a) Is Over-Expressed during Prion Disease and Modulates the Innate Immune Response and the Microglial Activation State

              Reuben Saba, Shantel Gushue, Rhiannon L. C. H. Huzarewich … (2012)
              Increasing evidence supports the involvement of microRNAs (miRNAs) in inflammatory and immune processes in prion neuropathogenesis. MiRNAs are small, non-coding RNA molecules which are emerging as key regulators of numerous cellular processes. We established miR-146a over-expression in prion-infected mouse brain tissues concurrent with the onset of prion deposition and appearance of activated microglia. Expression profiling of a variety of central nervous system derived cell-lines revealed that miR-146a is preferentially expressed in cells of microglial lineage. Prominent up-regulation of miR-146a was evident in the microglial cell lines BV-2 following TLR2 or TLR4 activation and also EOC 13.31 via TLR2 that reached a maximum 24–48 hours post-stimulation, concomitant with the return to basal levels of transcription of induced cytokines. Gain- and loss-of-function studies with miR-146a revealed a substantial deregulation of inflammatory response pathways in response to TLR2 stimulation. Significant transcriptional alterations in response to miR-146a perturbation included downstream mediators of the pro-inflammatory transcription factor, nuclear factor-kappa B (NF-κB) and the JAK-STAT signaling pathway. Microarray analysis also predicts a role for miR-146a regulation of morphological changes in microglial activation states as well as phagocytic mediators of the oxidative burst such as CYBA and NOS3. Based on our results, we propose a role for miR-146a as a potent modulator of microglial function by regulating the activation state during prion induced neurodegeneration.
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                Author and article information

                Journal
                Journal ID (iso-abbrev): J Neuroinflammation
                Title: Journal of neuroinflammation
                Publisher: Springer Science and Business Media LLC
                ISSN (Electronic): 1742-2094
                ISSN (Print): 1742-2094
                Publication date (Electronic): Feb 18 2015
                Volume: 12
                Affiliations
                [1 ] Laboratory of Neurovirology and Inflammation Biology, CSIR-Centre for Cellular and Molecular Biology (CCMB), Uppal Road, 500007, Hyderabad, AP, India. nikhil@ccmb.res.in.
                [2 ] Laboratory of Neurovirology and Inflammation Biology, CSIR-Centre for Cellular and Molecular Biology (CCMB), Uppal Road, 500007, Hyderabad, AP, India. ruhiverma78@gmail.com.
                [3 ] National Brain Research Centre, Haryana-122050, Manesar, Haryana, India. kanhaiya81@gmail.com.
                [4 ] National Brain Research Centre, Haryana-122050, Manesar, Haryana, India. anirban@nbrc.ac.in.
                [5 ] Laboratory of Neurovirology and Inflammation Biology, CSIR-Centre for Cellular and Molecular Biology (CCMB), Uppal Road, 500007, Hyderabad, AP, India. sunitsingh2000@gmail.com.
                [6 ] Current Affiliation: Laboratory of Human Molecular Virology and Immunology, Molecular Biology Unit, Faculty of Medicine, Institute of Medical Sciences (IMS), Banaras Hindu University (BHU), 221005, Varanasi, India. sunitsingh2000@gmail.com.
                Article
                Publisher Item ID: 10.1186/s12974-015-0249-0
                DOI: 10.1186/s12974-015-0249-0
                PMC ID: 4355369
                PubMed ID: 25889446
                SO-VID: 6b803264-5a5a-4580-968c-fbc70dbc7ce6
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