About: Alisporivir Inhibition of Hepatocyte Cyclophilins Reduces HBV Replication and Hepatitis B Surface Antigen Production

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About: Alisporivir Inhibition of Hepatocyte Cyclophilins Reduces HBV Replication and Hepatitis B Surface Antigen Production Goto Sponge NotDistinct Permalink

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

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type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
title	Alisporivir Inhibition of Hepatocyte Cyclophilins Reduces HBV Replication and Hepatitis B Surface Antigen Production
Creator	Gallay, Philippe Chatterji, Udayan Bobardt, Michael Williams, Roger Chokshi, Shilpa Naoumov, Nikolai Phillips, Sandra Riva, Antonio
source	Elsevier; Medline; PMC
abstract	Background & Aims Cyclophilins are host factors required for hepatitis C virus replication. Cyclophilin inhibitors such as alisporivir have shown strong anti–hepatitis C virus activity in vitro and in clinical studies. However, little is known about whether hepatocyte cyclophilins are involved in the hepatitis B virus (HBV) life cycle. We investigated the effects of 2 cyclophilin inhibitors (alisporivir and NIM811) on HBV replication and hepatitis B surface antigen (HBsAg) production in cell lines. Methods Liver-derived cell lines producing full-length HBV and HBsAg particles, owing to stable (HepG2215) or transient (HuH-7) transfection, or infected with HBV (HepaRG cells; Invitrogen [Carlsbad, CA]), were incubated with alisporivir or NIM811 alone, or alisporivir in combination with a direct antiviral (telbivudine). The roles of individual cyclophilins in drug response was evaluated by small interfering RNA knockdown of cyclophilin (CYP)A, CYPC, or CYPD in HepG2215 cells, or CYPA knockdown in HuH-7 cells. The kinetics of antiviral activity were assessed based on levels of HBV DNA and HBsAg and Southern blot analysis. Results In HepG2215, HuH-7, and HepaRG cells, alisporivir reduced intracellular and secreted HBV DNA, in a dose-dependent manner. Knockdown of CYPA, CYPC, or CYPD (reduced by 80%) significantly reduced levels of HBV DNA and secreted HBsAg. Knockdown of CYPA significantly reduced secretion of HBsAg, leading to accumulation of intracellular HBsAg; the addition of alisporivir greatly reduced levels of HBsAg in these cells. The combination of alisporivir and telbivudine had greater antiviral effects than those of telbivudine or alisporivir alone. Conclusions Alisporivir inhibition of cyclophilins in hepatocyte cell lines reduces replication of HBV DNA and HBsAg production and secretion. These effects are potentiated in combination with direct antiviral agents that target HBV-DNA polymerase.
has issue date	2015-02-28(xsd:dateTime)
bibo:doi	10.1053/j.gastro.2014.10.004
bibo:pmid	25305505
has license	els-covid
sha1sum (hex)	7b95b96d1faf8d2fb5324ca5d068ff081be6eff1
schema:url	https://doi.org/10.1053/j.gastro.2014.10.004
resource representing a document's title	Alisporivir Inhibition of Hepatocyte Cyclophilins Reduces HBV Replication and Hepatitis B Surface Antigen Production
has PubMed Central identifier	PMC7172380
has PubMed identifier	25305505
schema:publication	Gastroenterology
resource representing a document's body	covid:7b95b96d1faf8d2fb5324ca5d068ff081be6eff1#body_text
is schema:about of	named entity 'Hepatitis B' named entity 'enzymatic activity' named entity 'nucleocapsid' named entity 'hepatocytes' named entity 'nmol/L' named entity 'telbivudine' named entity 'HuH-7' named entity 'HBsAg' named entity 'siRNA' named entity 'selection marker' named entity 'CYPA' named entity 'secretion' named entity 'HBsAg' named entity 'HBV' named entity 'plasmid' named entity 'HuH-7' named entity 'siRNA' named entity 'antiviral effect' named entity 'Mountain View' named entity 'CYPA' named entity 'apolipoprotein' named entity 'intracellular' named entity 'HBsAg' named entity 'NIM811' named entity 'HuH-7' named entity 'lipids' named entity 'HBV' named entity 'chronic hepatitis' named entity 'cyclophilins' named entity 'hepatitis B surface' named entity 'HuH-7' named entity 'sodium taurocholate' named entity 'cyclophilin' named entity 'NIM811' named entity 'HuH-7' named entity 'CYPA' named entity 'Applied Biosystems' named entity 'intracellular' named entity 'NIM811' named entity 'HBV' named entity 'siRNA' named entity 'coronaviruses' named entity 'HuH-7' named entity 'intracellular' named entity 'CYPA' named entity 'CYPA' named entity 'HBsAg' named entity 'polymerase' named entity 'Invitrogen' named entity 'transfected' named entity 'mRNA' named entity 'CYPA' named entity 'transfection' named entity 'cyclophilin' named entity 'clinical studies' named entity 'nucleoside analog' named entity 'HuH-7' named entity 'prolyl isomerase' named entity 'DNA polymerase' named entity 'NIM811' named entity 'HBV' named entity 'collagen' named entity 'siRNA' named entity 'cell line' named entity 'HBsAg' named entity 'antiviral agent' named entity 'HBV' named entity 'HBV' named entity 'antiviral activity' named entity 'HBsAg' named entity 'hepatocytes' named entity 'life cycle' named entity 'Invitrogen' named entity 'polymerase'

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