About: Fast type I interferon response protects astrocytes from flavivirus infection and virus-induced cytopathic effects

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About: Fast type I interferon response protects astrocytes from flavivirus infection and virus-induced cytopathic effects Goto Sponge NotDistinct Permalink

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

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Fast type I interferon response protects astrocytes from flavivirus infection and virus-induced cytopathic effects
Creator	Lindqvist, Richard Kröger, Andrea Mundt, Filip Wölfel, Silke Gekara, Nelson Gilthorpe, Jonathan
Source	Medline; PMC
abstract	BACKGROUND: Neurotropic flaviviruses such as tick-borne encephalitis virus (TBEV), Japanese encephalitis virus (JEV), West Nile virus (WNV), and Zika virus (ZIKV) are causative agents of severe brain-related diseases including meningitis, encephalitis, and microcephaly. We have previously shown that local type I interferon response within the central nervous system (CNS) is involved in the protection of mice against tick-borne flavivirus infection. However, the cells responsible for mounting this protective response are not defined. METHODS: Primary astrocytes were isolated from wild-type (WT) and interferon alpha receptor knock out (IFNAR(−/−)) mice and infected with neurotropic flaviviruses. Viral replication and spread, IFN induction and response, and cellular viability were analyzed. Transcriptional levels in primary astrocytes treated with interferon or supernatant from virus-infected cells were analyzed by RNA sequencing and evaluated by different bioinformatics tools. RESULTS: Here, we show that astrocytes control viral replication of different TBEV strains, JEV, WNV, and ZIKV. In contrast to fibroblast, astrocytes mount a rapid interferon response and restrict viral spread. Furthermore, basal expression levels of key interferon-stimulated genes are high in astrocytes compared to mouse embryonic fibroblasts. Bioinformatic analysis of RNA-sequencing data reveals that astrocytes have established a basal antiviral state which contributes to the rapid viral recognition and upregulation of interferons. The most highly upregulated pathways in neighboring cells were linked to type I interferon response and innate immunity. The restriction in viral growth was dependent on interferon signaling, since loss of the interferon receptor, or its blockade in wild-type cells, resulted in high viral replication and virus-induced cytopathic effects. Astrocyte supernatant from TBEV-infected cells can restrict TBEV growth in astrocytes already 6 h post infection, the effect on neurons is highly reinforced, and astrocyte supernatant from 3 h post infection is already protective. CONCLUSIONS: These findings suggest that the combination of an intrinsic constitutive antiviral response and the fast induction of type I IFN production by astrocytes play an important role in self-protection of astrocytes and suppression of flavivirus replication in the CNS. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12974-016-0748-7) contains supplementary material, which is available to authorized users.
has issue date	2016-10-24(xsd:dateTime)
bibo:doi	10.1186/s12974-016-0748-7
bibo:pmid	27776548
has license	cc-by
sha1sum (hex)	96a89e5c0df1a32d5e2864966057fab04d2e3a23
schema:url	https://doi.org/10.1186/s12974-016-0748-7
resource representing a document's title	Fast type I interferon response protects astrocytes from flavivirus infection and virus-induced cytopathic effects
has PubMed Central identifier	PMC5078952
has PubMed identifier	27776548
schema:publication	J Neuroinflammation
resource representing a document's body	covid:96a89e5c0df1a32d5e2864966057fab04d2e3a23#body_text
is schema:about of	named entity 'bioinformatics' named entity 'levels' named entity 'VIRUS' named entity 'INTERFERON ' named entity 'RESPONSE' named entity 'TYPE I INTERFERON' named entity 'RESPONSIBLE' named entity 'BIOINFORMATICS' named entity 'SUPERNATANT' named entity 'ZIKA VIRUS' covid:arg/96a89e5c0df1a32d5e2864966057fab04d2e3a23 named entity 'CYTOPATHIC EFFECTS' named entity 'PRIMARY' named entity 'FLAVIVIRUS INFECTION' named entity 'TREATED WITH' named entity 'CELLS' named entity 'PROTECTION' named entity 'WILD-TYPE' named entity 'VIRAL REPLICATION' named entity 'WEST NILE VIRUS' named entity 'RNA SEQUENCING' named entity 'TRANSCRIPTIONAL' named entity 'INDUCED' named entity 'RESPONSE' named entity 'ASTROCYTES' named entity 'FAST' named entity 'FLAVIVIRUS INFECTION' named entity 'CAUSATIVE AGENTS' named entity 'VIABILITY' named entity 'NOT DEFINED' named entity 'SPREAD' named entity 'MICE' named entity 'TOOLS' named entity 'INTERFERON ALPHA RECEPTOR' named entity 'ASTROCYTES' named entity 'TICK-BORNE ENCEPHALITIS VIRUS' named entity 'CELLULAR' named entity 'DISEASES' named entity 'LEVELS' named entity 'MOUNTING' named entity 'INFECTED' named entity 'TICK-BORNE FLAVIVIRUS' named entity 'HAVE' named entity 'MICROCEPHALY' named entity 'DIFFERENT' named entity 'BRAIN' named entity 'RELATED' named entity 'LOCAL' named entity 'FLAVIVIRUSES' named entity 'INCLUDING' named entity 'ANALYZED' named entity 'INDUCTION' named entity 'METHODS' named entity 'ISOLATED' named entity 'INTERFERON ' named entity 'INVOLVED' named entity 'ENCEPHALITIS' named entity 'KNOCK OUT' named entity 'JAPANESE ENCEPHALITIS VIRUS' named entity 'EVALUATED' named entity 'MENINGITIS' named entity 'NEUROTROPIC' named entity 'SEVERE' named entity 'CENTRAL NERVOUS SYSTEM' named entity 'TYPE I INTERFERON' named entity 'IFN' named entity 'PREVIOUSLY' named entity 'BACKGROUND' named entity 'VIRUS' named entity 'cells' named entity 'IFN' named entity 'cellular' named entity 'receptor' named entity 'interferon' named entity 'JEV' named entity 'tick-borne encephalitis virus'

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