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Infectious Disease: Hepatitis C

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Total 109 results found since Jan 2013.

RacGTPase-activating protein 1 interacts with hepatitis C virus polymerase NS5B to regulate viral replication.
Abstract Hepatitis C virus (HCV) is a positive-strand RNA virus responsible for chronic liver disease and hepatocellular carcinoma (HCC). Rac GTPase-activating protein 1 (RacGAP1) plays an important role during GTP hydrolysis to GDP in Rac1 and CDC42 protein and has been demonstrated to be upregulated in several cancers, including HCC. However, the molecular mechanism leading to the upregulation of RacGAP1 remains poorly understood. Here, we showed that RacGAP1 levels were enhanced in HCV cell-culture-derived (HCVcc) infection. More importantly, we illustrated that RacGAP1 interacts with the viral protein NS5B in ...
Source: Biochemical and Biophysical Research communications - October 8, 2014 Category: Biochemistry Authors: Wu MJ, Ke PY, Horng JT Tags: Biochem Biophys Res Commun Source Type: research

Rab13 Is Involved in the Entry Step of Hepatitis C Virus Infection.
Abstract Membrane transport probably participates in the lifecycle of hepatitis C virus (HCV). Rab proteins are essential host factors for HCV RNA replication, but these proteins' roles in other steps of the HCV lifecycle are not clear. The tight junction (TJ) plays a key role in HCV infection. Rab13 regulates the endocytic recycling of the TJ-associated proteins. Here we investigated whether Rab13 is involved in the HCV entry step. We used HuH-7-derived RSc cells and Li23-derived D7 cells. To evaluate the effect of Rab13 in HCV infection, we transfected the cells with siRNA targeting Rab13 before HCV infection. T...
Source: Acta Med Okayama - March 31, 2016 Category: Universities & Medical Training Authors: Takeda M, Ikeda M, Satoh S, Dansako H, Wakita T, Kato N Tags: Acta Med Okayama Source Type: research

Inhibitory effect of miR-125b on hepatitis C virus core protein-induced TLR2/MyD88 signaling in THP-1 cells.
CONCLUSION: The inverse correlation between miR-125b and cytokine expression after HCV core challenge suggests that miR-125b may negatively regulate HCV-induced immune responses by targeting TLR2/MyD88 signaling in monocytes. PMID: 27158204 [PubMed - in process]
Source: World Journal of Gastroenterology : WJG - May 6, 2016 Category: Gastroenterology Authors: Peng C, Wang H, Zhang WJ, Jie SH, Tong QX, Lu MJ, Yang DL Tags: World J Gastroenterol Source Type: research

The Antiviral Role of Zinc and Metallothioneins in Hepatitis C Infection
This article is protected by copyright. All rights reserved.
Source: Journal of Viral Hepatitis - December 1, 2017 Category: Infectious Diseases Authors: Scott A Read, Grant Parnell, David Booth, Mark W Douglas, Jacob George, Golo Ahlenstiel Tags: Original Paper Source Type: research

The IL-6/STAT3 pathway upregulates microRNA-125b expression in hepatitis C virus infection.
Conclusions: This study elucidates a novel pathway for miR-125b in the pathogenesis of chronic HCV infection and suggests it as a possible target for treating HCV infection. PMID: 29541414 [PubMed]
Source: Oncotarget - March 16, 2018 Category: Cancer & Oncology Tags: Oncotarget Source Type: research

Caffeic acid inhibits HCV replication via induction of IFN α antiviral response through p62-mediated Keap1/Nrf2 signaling pathway
In this study, we showed that CA could notably inhibit HCV replication. Mechanism study demonstrated that CA could induce HO-1 expression, which would trigger the IFNα antiviral response, and the antiviral effect of CA was attenuated when HO-1 activity was inhibited by SnPP (an HO-1 inhibitor). CA could also increase erythroid 2-related factor 2 (Nrf2) expression. When Nrf2 was knocked down by specific siRNA, HO-1 expression was concomitantly decreased while HCV expression was restored. Further study indicated that kelch-like ECH-associated protein 1 (Keap1) expression was decreased by CA in a p62/Sequestosome1 (p62)-depe...
Source: Antiviral Therapy - April 14, 2018 Category: Virology Source Type: research

Caffeic acid inhibits HCV replication via induction of IFN α antiviral response through p62-mediated Keap1/Nrf2 signaling pathway.
In this study, we showed that CA could notably inhibit HCV replication. Mechanism study demonstrated that CA could induce HO-1 expression, which would trigger the IFNα antiviral response, and the antiviral effect of CA was attenuated when HO-1 activity was inhibited by SnPP (an HO-1 inhibitor). CA could also increase erythroid 2-related factor 2 (Nrf2) expression. When Nrf2 was knocked down by specific siRNA, HO-1 expression was concomitantly decreased while HCV expression was restored. Further study indicated that kelch-like ECH-associated protein 1 (Keap1) expression was decreased by CA in a p62/Sequestosome1 (p62)-depe...
Source: Antiviral Research - April 12, 2018 Category: Virology Authors: Shen J, Wang G, Zuo J Tags: Antiviral Res Source Type: research

Characterization of In vitro inhibitory effects of consensus short interference RNAs against non-structural 5B gene of hepatitis C virus 1a genotype
Conclusions: Stable Huh-7 cells persistently expressing NS5B protein should be helpful for molecular pathogenesis of HCV infection and development of anti-HCV drug screening assays. The siRNA was effective against NS5B and could be considered as an adjuvant therapy along with other promising anti-HCV regimens.
Source: Indian Journal of Medical Microbiology - March 17, 2019 Category: Microbiology Authors: Imran Shahid Waleed Hassan Almalki Munjed M Ibrahim Sultan Ahmad Alghamdi Mohammed H Mukhtar Shaia Saleh R. Almalki Saad Ahmed Alkahtani Mohammad S Alhaidari Source Type: research

SOCS and Herpesviruses, With Emphasis on Cytomegalovirus Retinitis
Christine I. Alston1,2 and Richard D. Dix1,2* 1Department of Biology, Viral Immunology Center, Georgia State University, Atlanta, GA, United States 2Department of Ophthalmology, Emory University School of Medicine, Atlanta, GA, United States Suppressor of cytokine signaling (SOCS) proteins provide selective negative feedback to prevent pathogeneses caused by overstimulation of the immune system. Of the eight known SOCS proteins, SOCS1 and SOCS3 are the best studied, and systemic deletion of either gene causes early lethality in mice. Many viruses, including herpesviruses such as herpes simplex virus and cytomega...
Source: Frontiers in Immunology - April 10, 2019 Category: Allergy & Immunology Source Type: research

Transcription Factor MafB Suppresses Type I Interferon Production by CD14+ Monocytes in Patients With Chronic Hepatitis C
Transcription factor MafB regulates differentiation and activity of monocytes/macrophage, and is associated with the development of atherosclerosis and cancers. However, the role of MafB in modulation of CD14+ monocytes in chronic viral hepatitis was not fully elucidated. Thus, the aim of current study was to investigate the immunoregulatory function of MafB to type I interferon (IFN) secretion by CD14+ monocytes and its contribution to pathogenesis of chronic hepatitis C virus (HCV) infection. A total of twenty-nine chronic hepatitis C patients and twenty-one healthy individuals were enrolled. Serum IFN-α1 and IFN-β was...
Source: Frontiers in Microbiology - August 6, 2019 Category: Microbiology Source Type: research

A 7-Amino Acid Peptide Mimic from Hepatitis C Virus Hypervariable Region 1 Inhibits Mouse Lung Th9 Cell Differentiation by Blocking CD81 Signaling during Allergic Lung Inflammation.
Authors: Zhao W, Tan C, Yu X, Yu R, Mei Q, Cheng Y Abstract T helper (Th) cells orchestrate allergic lung inflammation in asthma pathogenesis. Th9 is a novel Th cell subset that mainly produces IL-9, a potent proinflammatory cytokine in asthma. A 7-amino acid peptide (7P) of the hypervariable region 1 (HVR1) of hepatitis C virus has been identified as an important regulator in the type 2 cytokine (IL-4, IL-5, and IL-13) immune response. However, it is unknown whether 7P regulates Th9 cell differentiation during ovalbumin- (OVA-) induced allergic lung inflammation. To address this, we studied wild-type mice treated ...
Source: Journal of Immunology Research - April 8, 2020 Category: Allergy & Immunology Tags: J Immunol Res Source Type: research

Transfection efficacy and drug release depends upon the PEG derivative in cationic lipoplexes: Evaluation in 3D in vitro model and in vivo
J Biomed Mater Res B Appl Biomater. 2023 May 3. doi: 10.1002/jbm.b.35259. Online ahead of print.ABSTRACTThe goal of the study was to estimate transfection efficacy and drug release in function of the PEG derivative in cationic liposomes and lipoplexes in both 2D and 3D in vitro models as well as in a mouse model (in vivo). For this purpose, cationic PEGylated nanocarriers based on OrnOrnGlu(C16 H33 )2 lipopeptides were fabricated and characterized. The nanocarriers were loaded with DNA plasmid pGL3 or with siRNA targeting 5'-UTR region of Hepatitis C virus, and their transfection efficacies were studied by luciferase test ...
Source: Biomed Res - May 3, 2023 Category: Research Authors: Gileva A M Koloskova O O Nosova A S Vishniakova L I Simonova V A Kurbanova L A Egorenkov E A Smirnov V V Budanova U A Sebyakin Yu L Suzina N E Khaitov M R Markvicheva E Source Type: research

The modulation of hepatitis C virus 1a replication by PKR is dependent on NF-kB mediated interferon beta response in Huh7.5.1 cells.
Abstract Protein kinase R (PKR), a sensor of double-stranded RNA, plays an important role in the host response to viral infection. Hepatitis C genotype 2a virus (HCV2a) has been shown to induce PKR activation to suppress the translation of antiviral interferon stimulated genes (ISGs), suggesting that PKR inhibitor can be beneficial for treating chronically HCV-infected patients in conjunction with interferon alpha and ribavirin. However, in this study, we found that PKR inhibition using siRNA PKR, shRNA PKR or PKR inhibitor enhanced HCV 1a replication and rendered Huh7.5.1 cells more susceptible to HCV1a infection...
Source: Virology - February 8, 2013 Category: Virology Authors: Zhang L, Alter HJ, Wang H, Jia S, Wang E, Marincola FM, Shih JW, Wang RY Tags: Virology Source Type: research