About: Inhibition of hepatitis C virus replication by chloroquine targeting virus-associated autophagy

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About: Inhibition of hepatitis C virus replication by chloroquine targeting virus-associated autophagy Goto Sponge NotDistinct Permalink

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type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Inhibition of hepatitis C virus replication by chloroquine targeting virus-associated autophagy
Creator	Tanida, Isei Sakamoto, Naoya Ae, Enomoto Ae, Ikejima Ae, Kominami Ae, Takashi Ae, Takei Ae, Yamashina Eiki, A Enomoto, N Ikejima, K Ikejima, Á Kenichi, A Kitamura, T Kitamura, Tsuneo Kitamura, Á Kominami, E Kominami, Á Mizui, T Mizui, Tomokazu Nobuyuki, A Sakai, T Sakai, Tatsuo Sakamoto, N Shunhei, A Takei, Y Tanida, I Ueno, T Watanabe, S Watanabe, Sumio Watanabe, Á Yamashina, S Yamashina, Á Yoshiyuki, A
Source	Medline; PMC
abstract	BACKGROUND: Autophagy has been reported to play a pivotal role on the replication of various RNA viruses. In this study, we investigated the role of autophagy on hepatitis C virus (HCV) RNA replication and demonstrated anti-HCV effects of an autophagic proteolysis inhibitor, chloroquine. METHODS: Induction of autophagy was evaluated following the transfection of HCV replicon to Huh-7 cells. Next, we investigated the replication of HCV subgenomic replicon in response to treatment with lysosomal protease inhibitors or pharmacological autophagy inhibitor. The effect on HCV replication was analyzed after transfection with siRNA of ATG5, ATG7 and light-chain (LC)-3 to replicon cells. The antiviral effect of chloroquine and/or interferon-α (IFNα) was evaluated. RESULTS: The transfection of HCV replicon increased the number of autophagosomes to about twofold over untransfected cells. Pharmacological inhibition of autophagic proteolysis significantly suppressed expression level of HCV replicon. Silencing of autophagy-related genes by siRNA transfection significantly blunted the replication of HCV replicon. Treatment of replicon cells with chloroquine suppressed the replication of the HCV replicon in a dose-dependent manner. Furthermore, combination treatment of chloroquine to IFNα enhanced the antiviral effect of IFNα and prevented re-propagation of HCV replicon. Protein kinase R was activated in cells treated with IFNα but not with chloroquine. Incubation with chloroquine decreased degradation of long-lived protein leucine. CONCLUSION: The results of this study suggest that the replication of HCV replicon utilizes machinery involving cellular autophagic proteolysis. The therapy targeted to autophagic proteolysis by using chloroquine may provide a new therapeutic option against chronic hepatitis C.
has issue date	2009-09-17(xsd:dateTime)
bibo:doi	10.1007/s00535-009-0132-9
bibo:pmid	19760134
has license	no-cc
sha1sum (hex)	6098130a6b009a803ce4abeb2bb4d2636ee6c573
schema:url	https://doi.org/10.1007/s00535-009-0132-9
resource representing a document's title	Inhibition of hepatitis C virus replication by chloroquine targeting virus-associated autophagy
has PubMed Central identifier	PMC7088329
has PubMed identifier	19760134
schema:publication	J Gastroenterol
resource representing a document's body	covid:6098130a6b009a803ce4abeb2bb4d2636ee6c573#body_text
is schema:about of	named entity 'ASSOCIATED' named entity 'demonstrated' named entity 'hepatitis C virus' named entity 'RNA VIRUSES' named entity 'BACKGROUND' named entity 'PLAY' named entity 'ATG7' named entity 'EVALUATED' named entity 'REPLICON' named entity 'LYSOSOMAL' named entity 'LIGHT-CHAIN' named entity 'AUTOPHAGY' named entity 'SIRNA' named entity 'VARIOUS' named entity 'ATG5' named entity 'TRANSFECTION' named entity 'CHLOROQUINE' named entity 'HCV' named entity 'RESPONSE TO TREATMENT' named entity 'REPORTED' named entity 'FOLLOWING' named entity 'CHLOROQUINE' named entity 'REPLICATION' named entity 'EFFECT' named entity 'PROTEASE INHIBITORS' named entity 'METHODS' named entity 'EFFECTS' named entity 'VIRUS REPLICATION' named entity 'INHIBITION' named entity 'PROTEOLYSIS' named entity 'ANTIVIRAL' named entity 'STUDY' named entity 'VIRUS' named entity 'HEPATITIS C VIRUS' named entity 'AUTOPHAGY' named entity 'TARGETING' named entity 'INHIBITOR' named entity 'INVESTIGATED' named entity 'DEMONSTRATED' named entity 'CELLS' named entity 'RNA REPLICATION' named entity 'HEPATITIS C VIRUS' named entity 'ROLE' named entity 'HUH-7' named entity 'AUTOPHAGY INHIBITOR' named entity 'ANALYZED' named entity 'PHARMACOLOGICAL' named entity 'INDUCTION'

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