About: Induction of Atypical Autophagy by Porcine Hemagglutinating Encephalomyelitis Virus Contributes to Viral Replication

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About: Induction of Atypical Autophagy by Porcine Hemagglutinating Encephalomyelitis Virus Contributes to Viral Replication 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	Induction of Atypical Autophagy by Porcine Hemagglutinating Encephalomyelitis Virus Contributes to Viral Replication
Creator	Gao, Feng He, Wenqi Lan, Yungang Lu, Huijun Zhao, Kui Ding, Ning Li, Zi Lv, Xiaoling Su, Jingjing Wang, Penghua Garzino-Demo, Alfredo Perfumo, Carlos
Source	Medline; PMC
abstract	Autophagy is a basic biological metabolic process involving in intracellular membrane transport pathways that recycle cellular components and eliminate intracellular microorganisms within the lysosome. Autophagy also plays an important part in virus infection and propagation. However, some pathogens, including viruses, have evolved unique trick to escape or exploit autophagy. This study explores the mechanism of autophagy induction by porcine hemagglutinating encephalomyelitis virus (PHEV) in Neuro-2a cells, and examines the role of autophagy in PHEV replication. PHEV triggered autophagy in Neuro-2a cells is dependent on the presence of bulk double- or single-membrane vacuoles, the accumulation of GFP-LC3 fluorescent dots, and the LC3 lipidation. In addition, PHEV induced an incomplete autophagic effect because the degradation level of p62 did not change in PHEV-infected cells. Further validation was captured using LysoTracker and lysosome-associated membrane protein by indirect immunofluorescence labeling in PHEV-infected cells. We also investigated the change in viral replication by pharmacological experiments with the autophagy inducer rapamycin or the autophagy inhibitor 3-MA, and the lysosomal inhibitor chloroquine (CQ). Suppression of autophagy by 3-MA increased viral replication, compared with the mock treatment, while promoting of autophagy by rapamycin reduced PHEV replication. CQ treatment enhanced the LC3 lipidation in PHEV-infected Neuro-2a cells but lowered PHEV replication. These results show that PHEV infection induces atypical autophagy and causes the appearance of autophagosomes but blocks the fusion with lysosomes, which is necessary for the replication of PHEV in nerve cells.
has issue date	2017-02-28(xsd:dateTime)
bibo:doi	10.3389/fcimb.2017.00056
bibo:pmid	28293544
has license	cc-by
sha1sum (hex)	c4b7ab00946639c33eebee571e31d74e2543de95
schema:url	https://doi.org/10.3389/fcimb.2017.00056
resource representing a document's title	Induction of Atypical Autophagy by Porcine Hemagglutinating Encephalomyelitis Virus Contributes to Viral Replication
has PubMed Central identifier	PMC5328988
has PubMed identifier	28293544
schema:publication	Front Cell Infect Microbiol
resource representing a document's body	covid:c4b7ab00946639c33eebee571e31d74e2543de95#body_text
is schema:about of	named entity 'VIRAL REPLICATION' named entity 'viruses' named entity 'chloroquine' named entity 'encephalomyelitis' named entity 'enhanced' named entity 'inhibitor' named entity 'PHEV' named entity 'experiments' named entity 'induction' covid:arg/c4b7ab00946639c33eebee571e31d74e2543de95 named entity 'NERVE CELLS' named entity 'LC3' named entity 'RECYCLE' named entity 'EXPLOIT' named entity 'THESE' named entity 'BASIC' named entity 'LYSOSOME-ASSOCIATED MEMBRANE PROTEIN' named entity 'PLAYS' named entity 'ACCUMULATION' named entity 'PORCINE HEMAGGLUTINATING ENCEPHALOMYELITIS VIRUS' named entity 'VIRUSES' named entity 'SUPPRESSION' named entity 'INTRACELLULAR MEMBRANE' named entity 'INFECTION' named entity 'INHIBITOR' named entity 'PROMOTING' named entity 'INDIRECT IMMUNOFLUORESCENCE' named entity 'MICROORGANISMS' named entity 'FLUORESCENT' named entity 'INFECTED' named entity 'AUTOPHAGY' named entity 'BIOLOGICAL' named entity 'COMPARED' named entity 'REDUCED' named entity 'ROLE' named entity 'DID' named entity 'BUT' named entity 'MOCK' named entity 'NECESSARY' named entity 'PRESENCE OF' named entity 'INTRACELLULAR' named entity 'USING' named entity 'BLOCKS' named entity 'METABOLIC PROCESS' named entity 'LYSOSOME' named entity 'AUTOPHAGY INDUCER' named entity 'RAPAMYCIN' named entity 'MEMBRANE TRANSPORT' named entity 'INDUCTION' named entity 'ADDITION' named entity 'INCLUDING' named entity 'HAVE' named entity 'EXPERIMENTS' named entity 'ENHANCED' named entity 'BULK' named entity 'DOTS' named entity 'DEGRADATION' named entity 'CHANGE IN' named entity 'AUTOPHAGY' named entity 'TREATMENT' named entity 'EFFECT' named entity 'CHLOROQUINE' named entity 'INVESTIGATED' named entity 'ATYPICAL' named entity 'REPLICATION' named entity 'UNIQUE' named entity 'LABELING' named entity 'CELLULAR' named entity 'THE CHANGE' named entity 'IS A'

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