About: Chemokine profiling of Japanese encephalitis virus-infected mouse neuroblastoma cells by microarray and real-time RT-PCR: Implication in neuropathogenesis

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About: Chemokine profiling of Japanese encephalitis virus-infected mouse neuroblastoma cells by microarray and real-time RT-PCR: Implication in neuropathogenesis Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : covidontheweb.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Chemokine profiling of Japanese encephalitis virus-infected mouse neuroblastoma cells by microarray and real-time RT-PCR: Implication in neuropathogenesis
Creator	Gupta, Nimesh Parida, M Rao, P Pradeep Babu, J Santhosh, S
Source	Elsevier; Medline; PMC
abstract	Abstract Japanese encephalitis (JE) is one of the leading causes of acute encephalopathy affecting children and adolescents in the tropics. JE virus (JEV) infection causes prominent neurological sequelae in approximately one-third of the survivors. In humans, the inflammatory response of CNS consequent to JEV induced viral encephalitis is mediated through chemokines released by various cells of CNS. In the present study, the chemokine profiles of mouse neuroblastoma cells (N2A) following JEV infection was analyzed by cDNA microarray followed by real-time RT-PCR. Eighty mRNA transcripts belonging to various functional classes exhibited significant alterations in gene expression. There was considerable induction of genes involved in apoptosis and anti-viral response. Modified levels of several transcripts involved in proinflammatory and anti-inflammatory processes exemplified the balance between opposing forces during JEV pathogenesis. Other genes displaying altered transcription included those associated with host translation, cellular metabolism, cell cycle, signal transduction, transcriptional regulation, protein trafficking, neurotransmitters, neuron maturation, protein modulators, ER stress and cytoskeletal proteins. The infection of neurons results in the synthesis of proinflammatory chemokines, which are early important mediators of leukocyte recruitment to sites of viral infection. Our results clearly suggest the implication of chemokines in neuropathogenesis of JEV infection leading to neurological sequelae. Pro- and anti-inflammatory agents targeted against chemokines such as CXCL10 may provide possible therapeutic modalities that can mitigate the morbidity associated with JEV infection of the CNS.
has issue date	2010-01-31(xsd:dateTime)
bibo:doi	10.1016/j.virusres.2009.10.018
bibo:pmid	19896511
has license	els-covid
sha1sum (hex)	b969dc0671344e9f8cca2ddf78d9fcb845f55cc9
schema:url	https://doi.org/10.1016/j.virusres.2009.10.018
resource representing a document's title	Chemokine profiling of Japanese encephalitis virus-infected mouse neuroblastoma cells by microarray and real-time RT-PCR: Implication in neuropathogenesis
has PubMed Central identifier	PMC7126115
has PubMed identifier	19896511
schema:publication	Virus Research
resource representing a document's body	covid:b969dc0671344e9f8cca2ddf78d9fcb845f55cc9#body_text
is schema:about of	named entity 'cytoskeletal proteins' named entity 'transcripts' named entity 'pathogenesis' named entity 'CNS' named entity 'provide' named entity 'cells' named entity 'mouse' named entity 'recruitment' named entity 'expression' named entity 'mRNA' named entity 'involved' named entity 'sites' named entity 'real-time' named entity 'RT-PCR' named entity 'CNS' named entity 'consequent' named entity 'mouse' named entity 'BELONGING' named entity 'GENE EXPRESSION' named entity 'NEURON MATURATION' named entity 'LEUKOCYTE RECRUITMENT' named entity 'INVOLVED' named entity 'ER STRESS' named entity 'MODULATORS' named entity 'APOPTOSIS' named entity 'POSSIBLE' named entity 'JAPANESE ENCEPHALITIS' named entity 'SITES' named entity 'ANTI-VIRAL RESPONSE' named entity 'ONE OF' named entity 'ADOLESCENTS' named entity 'SURVIVORS' named entity 'INFLAMMATORY RESPONSE' named entity 'FORCES' named entity 'ANTIINFLAMMATORY AGENTS' named entity 'INFECTION' named entity 'HUMANS' named entity 'MORBIDITY' named entity 'JAPANESE ENCEPHALITIS VIRUS' named entity 'CHEMOKINE' named entity 'TRANSCRIPTIONAL REGULATION' named entity 'TARGETED' named entity 'INCLUDED' named entity 'SUGGEST' named entity 'CONSEQUENT' named entity 'CELL CYCLE' named entity 'LEVELS' named entity 'NEUROBLASTOMA CELLS' named entity 'EARLY' named entity 'MICROARRAY' named entity 'NEUROBLASTOMA CELLS' named entity 'NEUROPATHOGENESIS' named entity 'REAL-TIME RT-PCR' named entity 'PRO-' named entity 'NEUROLOGICAL SEQUELAE' named entity 'ANTI-INFLAMMATORY' named entity 'FOLLOWING' named entity 'NEURONS' named entity 'CNS' named entity 'MEDIATORS' named entity 'MODALITIES' named entity 'APPROXIMATELY' named entity 'IMPORTANT' named entity 'MOUSE NEUROBLASTOMA' named entity 'CDNA MICROARRAY' named entity 'AFFECTING' named entity 'ALTERATIONS' named entity 'TRANSLATION' named entity 'CELLULAR METABOLISM' named entity 'FUNCTIONAL' named entity 'FOLLOWED BY' named entity 'CAUSES' named entity 'CHEMOKINES' named entity 'VIRUS' named entity 'NEUROPATHOGENESIS' named entity '2C CELL' named entity 'SIGNAL TRANSDUCTION'

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