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Hepatitis C virus lipids

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https://www.readbyqxmd.com/read/28729862/rad51-interacts-with-non-structural-3-protein-of-hepatitis-c-virus-and-regulates-viral-production
#1
Kidong Son, Tram T T Nguyen, Jae-Woong Choi, Long V Pham, Trang T D Luong, Yun-Sook Lim, Soon B Hwang
Hepatitis C virus (HCV) is a leading cause of chronic liver disease affecting over 170 million people worldwide. Chronic infection with HCV progresses to liver fibrosis, cirrhosis, and hepatocellular carcinoma. HCV exploits host cellular factors for viral propagation. To investigate the cellular factors required for HCV propagation, we screened a siRNA library targeting human cell cycle genes using cell culture grown HCV-infected cells. In the present study, we selected and characterized a gene encoding Rad51...
2017: Frontiers in Microbiology
https://www.readbyqxmd.com/read/28724915/quinolinate-phosphoribosyltransferase-is-an-antiviral-host-factor-against-hepatitis-c-virus-infection
#2
Zhilong Wang, Yanhang Gao, Chao Zhang, Haiming Hu, Dongwei Guo, Yi Xu, Qiuping Xu, Weihong Zhang, Sisi Deng, Pingyun Lv, Yan Yang, Yanhua Ding, Qingquan Li, Changjiang Weng, Xinwen Chen, Sitang Gong, Hairong Chen, Junqi Niu, Hong Tang
HCV infection can decrease NAD(+)/NADH ratio, which could convert lipid metabolism to favor HCV replication. In hepatocytes, quinolinate phosphoribosyl transferase (QPRT) catabolizes quinolinic acid (QA) to nicotinic acid mononucleotide (NAMN) for de novo NAD synthesis. However, whether and how HCV modulates QPRT hence the lipogenesis is unknown. In this work, we found QPRT was reduced significantly in livers of patients or humanized C/O(Tg) mice with persistent HCV infection. Mechanistic studies indicated that HCV NS3/4A promoted proteasomal degradation of QPRT through Smurf2, an E3 ubiquitin-protein ligase, in Huh7...
July 19, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28722331/hepatitis-c-virus-and-proprotein-convertase-subtilisin-kexin-type-9-a-detrimental-interaction-to-increase-viral-infectivity-and-disrupt-lipid-metabolism
#3
REVIEW
Matteo Pirro, Vanessa Bianconi, Daniela Francisci, Elisabetta Schiaroli, Francesco Bagaglia, Amirhossein Sahebkar, Franco Baldelli
From viral binding to the hepatocyte surface to extracellular virion release, the replication cycle of the hepatitis C virus (HCV) intersects at various levels with lipid metabolism; this leads to a derangement of the lipid profile and to increased viral infectivity. Accumulating evidence supports the crucial regulatory role of proprotein convertase subtilisin/kexin type 9 (PCSK9) in lipoprotein metabolism. Notably, a complex interaction between HCV and PCSK9 has been documented. Indeed, either increased or reduced circulating PCSK9 levels have been observed in HCV patients; this discrepancy might be related to several confounders, including HCV genotype, human immunodeficiency virus (HIV) coinfection and the ambiguous HCV-mediated influence on PCSK9 transcription factors...
July 18, 2017: Journal of Cellular and Molecular Medicine
https://www.readbyqxmd.com/read/28721844/cd81-large-extracellular-loop-containing-fusion-proteins-with-a-dominant-negative-effect-on-hcv-cell-spread-and-replication
#4
Boyan Grigorov, Jennifer Molle, Eric Rubinstein, Fabien Zoulim, Birke Bartosch
The roles of CD81 in the hepatitis C virus (HCV) life cycle are multiple but remain ill characterized. CD81 is known to interact with the HCV glycoproteins as an attachment factor. It also has an important role in the post-attachment entry process. Its interaction with claudin-1, for example, is vital for viral uptake and trafficking. Furthermore, CD81 and its role in membrane organization and trafficking are thought to play a pivotal role in HCV replication. Some of these functions are particularly limited to human CD81; others can be substituted with CD81 molecules from other species...
July 18, 2017: Journal of General Virology
https://www.readbyqxmd.com/read/28707319/tenofovir-disoproxil-fumarate-significantly-decreases-serum-lipoprotein-levels-compared-with-entecavir-nucleos-t-ide-analogue-therapy-in-chronic-hepatitis-b-carriers
#5
A A Shaheen, M AlMattooq, S Yazdanfar, K W Burak, M G Swain, S E Congly, M A Borman, S S Lee, R P Myers, C S Coffin
BACKGROUND: Tenofovir disoproxil fumarate (TDF) and entecavir (ETV) are first-line treatments for chronic hepatitis B (CHB). Studies suggest lipid lowering effect of TDF in human immunodeficiency virus positive (HIV+) individuals, but the effect on lipids and cardiovascular disease (CVD) risk in CHB is unknown. AIM: To compare TDF vs ETV effects on lipid levels in CHB. METHODS: In this retrospective cohort study, data on serum lipids and CVD risk factors at baseline and ~1 year on TDF or ETV were collected from CHB carriers...
July 13, 2017: Alimentary Pharmacology & Therapeutics
https://www.readbyqxmd.com/read/28689587/metabolic-manifestations-of-hepatitis-c-virus-diabetes-mellitus-dyslipidemia
#6
REVIEW
Lawrence Serfaty
Metabolic disorders are common in patients with chronic hepatitis C virus (HCV) infection. Epidemiologic and clinical data indicate an overprevalence of lipids abnormalite, steatosis, insuline resistance (IR) and diabetes mellitus in HCV patients, suggesting that HCV itself may interact with glucido-lipidic metabolism. HCV interacts with the host lipid metabolism by several mechanisms leading to hepatic steatosis and hypolipidemia which are reversible after viral eradication. Liver and peripheral IR are HCV genotype/viral load dependent and improved after viral eradication...
August 2017: Clinics in Liver Disease
https://www.readbyqxmd.com/read/28687362/the-unexpected-function-of-a-highly-conserved-yxx%C3%AE-motif-in-hcv-core-protein
#7
Eirini Karamichali, Elisavet Serti, Aikaterini Gianneli, Aikaterini Papaefthymiou, Athanassios Kakkanas, Pelagia Foka, Alexandros Seremetakis, Konstantina Katsarou, Ioannis P Trougakos, Urania Georgopoulou
Hepatitis C virus (HCV) is an RNA positive strand virus, member of the Flaviviridae family. The HCV viral particle is composed of a capsid containing the genome, surrounded by an endoplasmic reticulum (ER)-derived lipid bilayer where E1 and E2 are assembled as heterodimers. However, different forms of viral particles have been identified in the serum of HCV-infected patients, including non-enveloped particles. Previous reports have demonstrated that HCV non-enveloped capsid-like particles (HCVne) can be generated by HCV core protein sequence...
July 5, 2017: Infection, Genetics and Evolution
https://www.readbyqxmd.com/read/28663670/the-plasma-and-serum-metabotyping-of-hepatocellular-carcinoma-in-a-nigerian-and-egyptian-cohort-using-proton-nuclear-magnetic-resonance-spectroscopy
#8
Mohamed I F Shariff, Jin Un Kim, Nimzing G Ladep, Asmaa I Gomaa, Mary M E Crossey, Edith Okeke, Edmund Banwat, Imam Waked, I Jane Cox, Roger Williams, Elaine Holmes, Simon D Taylor-Robinson
BACKGROUND/AIMS: Previous studies have observed disturbances in the (1)H nuclear magnetic resonance (NMR) blood spectral profiles in malignancy. No study has metabotyped serum or plasma of hepatocellular carcinoma (HCC) patients from two diverse populations. We aimed to delineate the HCC patient metabotype from Nigeria (mostly hepatitis B virus infected) and Egypt (mostly hepatitis C virus infected) to explore lipid and energy metabolite alterations that may be independent of disease aetiology, diet and environment...
June 2017: Journal of Clinical and Experimental Hepatology
https://www.readbyqxmd.com/read/28660014/apolipoprotein-e-a-multifunctional-protein-with-implications-in-various-pathologies-as-a-result-of-its-structural-features
#9
REVIEW
Irina Florina Tudorache, Violeta Georgeta Trusca, Anca Violeta Gafencu
Apolipoprotein E (apoE), a 34 kDa glycoprotein, mediates hepatic and extrahepatic uptake of plasma lipoproteins and cholesterol efflux from lipid-laden macrophages. In humans, three structural different apoE isoforms occur, with subsequent functional changes and pathological consequences. Here, we review data supporting the involvement of apoE structural domains and isoforms in normal and altered lipid metabolism, cardiovascular and neurodegenerative diseases, as well as stress-related pathological states...
2017: Computational and Structural Biotechnology Journal
https://www.readbyqxmd.com/read/28657143/emergence-of-drug-resistance-associated-variants-and-changes-in-serum-lipid-profiles-in-sofosbuvir-plus-ledipasvir-treated-chronic-hepatitis-c-patients
#10
Hiromi Kan, Michio Imamura, Yoshiiku Kawakami, Kana Daijo, Yuji Teraoka, Fumi Honda, Yuki Nakamura, Kei Morio, Tomoki Kobayashi, Takashi Nakahara, Yuko Nagaoki, Tomokazu Kawaoka, Masataka Tsuge, Akira Hiramatsu, Hiroshi Aikata, C Nelson Hayes, Daiki Miki, Hidenori Ochi, Yoji Honda, Nami Mori, Shintaro Takaki, Keiji Tsuji, Kazuaki Chayama
Combination of sofosbuvir plus ledipasvir therapy has been expected to enhance sustained virological response (SVR) rates in hepatitis C virus (HCV) genotype 1 chronic infected patients. We analyzed the emergence of drug resistance-associated variants (RAVs) in treatment failure and changes in lipid profiles in sofosbuvir/ledipasvir-treated patients. 176 patients with chronic HCV genotype 1 infection without decompensated liver cirrhosis were treated with sofosbuvir/ledipasvir for 12 weeks. NS5A and NS5B RAVs were determined by either Invader assay or direct sequencing...
June 28, 2017: Journal of Medical Virology
https://www.readbyqxmd.com/read/28630011/interplay-between-hepatitis-c-virus-and-lipid-metabolism-during-virus-entry-and-assembly
#11
REVIEW
Muriel Lavie, Jean Dubuisson
Hepatitis C virus (HCV) infection is a major public health problem worldwide. In most cases, HCV infection becomes chronic, leading to the development of liver diseases that range from fibrosis to cirrhosis and hepatocellular carcinoma. Due to its medical importance, the HCV life cycle has been deeply characterized, and a unique feature of this virus is its interplay with lipids. Accordingly, all the steps of the virus life cycle are influenced by the host lipid metabolism. Indeed, due to their association with host lipoproteins, HCV particles have a unique lipid composition...
June 16, 2017: Biochimie
https://www.readbyqxmd.com/read/28625086/hepatitis-c-virus-apolipoprotein-interactions-molecular-mechanisms-and-clinical-impact
#12
Emilie Crouchet, Thomas F Baumert, Catherine Schuster
Chronic hepatitis C virus (HCV) infection is a leading cause of cirrhosis, hepatocellular carcinoma and liver failure. Moreover, chronic HCV infection is associated with liver steatosis and metabolic disorders. With 130-150 million people chronically infected in the world, HCV infection represents a major public health problem. One hallmark on the virus is its close link with hepatic lipid and lipoprotein metabolism. Areas covered: HCV is associated with lipoprotein components such as apolipoproteins. These interactions play a key role in the viral life cycle, viral persistence and pathogenesis of liver disease...
June 30, 2017: Expert Review of Proteomics
https://www.readbyqxmd.com/read/28623358/the-role-of-pten-hcv-core-interaction-in-hepatitis-c-virus-replication
#13
Qi Wu, Zhubing Li, Paul Mellor, Yan Zhou, Deborah H Anderson, Qiang Liu
Hepatitis C virus (HCV) infection leads to severe liver diseases including hepatocellular carcinoma (HCC). Phosphatase and tensin homolog deleted on chromosome 10 (PTEN), a tumour suppressor, is frequently mutated or deleted in HCC tumors. PTEN has previously been demonstrated to inhibit HCV secretion. In this study, we determined the effects of PTEN on the other steps in HCV life cycle, including entry, translation, and replication. We showed that PTEN inhibits HCV entry through its lipid phosphatase activity...
June 16, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28611396/coupling-neutron-reflectivity-with-cell-free-protein-synthesis-to-probe-membrane-protein-structure-in-supported-bilayers
#14
Thomas Soranzo, Donald K Martin, Jean-Luc Lenormand, Erik B Watkins
The structure of the p7 viroporin, an oligomeric membrane protein ion channel involved in the assembly and release of the hepatitis C virus, was determined from proteins expressed and inserted directly into supported model lipid membranes using cell-free protein expression. Cell-free protein expression allowed (i ) high protein concentration in the membrane, (ii ) control of the protein's isotopic constitution, and (iii ) control over the lipid environment available to the protein. Here, we used cell-free protein synthesis to directly incorporate the hepatitis C virus (HCV) p7 protein into supported lipid bilayers formed from physiologically relevant lipids (POPC or asolectin) for both direct structural measurements using neutron reflectivity (NR) and conductance measurements using electrical impedance spectroscopy (EIS)...
June 13, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28594932/ns5a-inhibitors-unmask-differences-in-functional-replicase-complex-half-life-between-different-hepatitis-c-virus-strains
#15
Tiffany Benzine, Ryan Brandt, William C Lovell, Daisuke Yamane, Petra Neddermann, Raffaele De Francesco, Stanley M Lemon, Alan S Perelson, Ruian Ke, David R McGivern
Hepatitis C virus (HCV) RNA is synthesized by the replicase complex (RC), a macromolecular assembly composed of viral non-structural proteins and cellular co-factors. Inhibitors of the HCV NS5A protein block formation of new RCs but do not affect RNA synthesis by pre-formed RCs. Without new RC formation, existing RCs turn over and are eventually lost from the cell. We aimed to use NS5A inhibitors to estimate the half-life of the functional RC of HCV. We compared different cell culture-infectious strains of HCV that may be grouped based on their sensitivity to lipid peroxidation: robustly replicating, lipid peroxidation resistant (LPOR) viruses (e...
June 2017: PLoS Pathogens
https://www.readbyqxmd.com/read/28587063/a-relative-deficiency-of-lysosomal-acid-lypase-activity-characterizes-non-alcoholic-fatty-liver-disease
#16
Francesco Tovoli, Lucia Napoli, Giulia Negrini, Sergio D'Addato, Giulia Tozzi, Jessica D'Amico, Fabio Piscaglia, Luigi Bolondi
Lysosomal acid lipase (LAL) is a key enzyme in lipid metabolism. Initial reports have suggested a role for a relative acquired LAL deficiency in non-alcoholic fatty liver disease (NAFLD)-however, it is still unclear whether this mechanism is specific for NAFLD. We aimed to determine LAL activity in a cohort of NAFLD subjects and in a control group of hepatitis C virus (HCV)-infected patients, investigating the role of liver cirrhosis. A total of 81 patients with a diagnosis of NAFLD, and 78 matched controls with HCV-related liver disease were enrolled...
May 25, 2017: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/28574577/pcsk9-and-infection-a-potentially-useful-or-dangerous-association
#17
REVIEW
Farzad Kahdemi, Amir Abbas Momtazi-Borojeni, Željko Reiner, Maciej Banach, Khalid Al Rasadi, Amirhossein Sahebkar
Elevated plasma low-density lipoprotein-cholesterol (LDL-C) concentration is the most important risk factor for atherosclerotic cardiovascular diseases. Proprotein convertase subtilisin/kexin type 9 (PCSK9) is a ubiquitously expressed serine proteinase which plays a key role in cholesterol metabolism, but has been found to be implicated in some other lipid-independent physiological processes. In this review, the role of PCSK9 was evaluated not only concerning lipid metabolism but also hepatitis C virus (HCV) infection, bacterial infections/sepsis and septic shock...
June 2, 2017: Journal of Cellular Physiology
https://www.readbyqxmd.com/read/28566716/glycogen-synthase-kinase-3%C3%AE-inhibitors-prevent-hepatitis-c-virus-release-assembly-through-perturbation-of-lipid-metabolism
#18
Mohammed A Sarhan, Mohamed S Abdel-Hakeem, Andrew L Mason, D Lorne Tyrrell, Michael Houghton
Direct acting antivirals against hepatitis C virus (HCV) have markedly improved cure rates in the past few years. However, they are expensive, with only few targeting host cell factors, and affecting virus assembly and release. Huh7.5 cells infected with a JFH-1 clone of HCV were treated with two different glycogen synthase kinase (GSK3)-β inhibitors; AR-A014418 and lithium chloride. Intra- and extracellular HCV virions and specific infectivity was determined using real-time RT-PCR and TCID50, and changes in lipid production were identified by enzyme-linked immunoassay and mass spectrometry analyses...
May 31, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28566381/hepatitis-c-virus-subverts-human-choline-kinase-%C3%AE-to-bridge-pi4kiii%C3%AE-and-ns5a-and-upregulates-pi4kiii%C3%AE-activation-thereby-promoting-the-translocation-of-the-ternary-complex-to-the-er-for-viral-replication
#19
Mun-Teng Wong, Steve S Chen
In this study, we elucidated the mechanism by which human choline kinase-α (hCKα) interacts with nonstructural protein (NS)5A and phosphatidylinositol-4-kinase (PI4K)IIIα, the lipid kinase crucial for maintaining the integrity of virus-induced membranous webs, and modulates hepatitis C virus (HCV) replication. hCKα activity positively modulated PI-4-phosphate (PI4P) levels in HCV-expressing cells, and hCKα-mediated PI4P accumulation was abolished by AL-9, a PI4KIIIα-specific inhibitor. hCKα colocalized with NS5A and PI4KIIIα or PI4P, NS5A expression increased hCKα and PI4KIIIα colocalization, and hCKα formed a ternary complex with PI4KIIIα and NS5A, supporting the functional interplay of hCKα with PI4KIIIα and NS5A...
May 31, 2017: Journal of Virology
https://www.readbyqxmd.com/read/28558013/downregulation-of-sirt1-signaling-underlies-hepatic-autophagy-impairment-in-glycogen-storage-disease-type-ia
#20
Jun-Ho Cho, Goo-Young Kim, Chi-Jiunn Pan, Javier Anduaga, Eui-Ju Choi, Brian C Mansfield, Janice Y Chou
A deficiency in glucose-6-phosphatase-α (G6Pase-α) in glycogen storage disease type Ia (GSD-Ia) leads to impaired glucose homeostasis and metabolic manifestations including hepatomegaly caused by increased glycogen and neutral fat accumulation. A recent report showed that G6Pase-α deficiency causes impairment in autophagy, a recycling process important for cellular metabolism. However, the molecular mechanism underlying defective autophagy is unclear. Here we show that in mice, liver-specific knockout of G6Pase-α (L-G6pc-/-) leads to downregulation of sirtuin 1 (SIRT1) signaling that activates autophagy via deacetylation of autophagy-related (ATG) proteins and forkhead box O (FoxO) family of transcriptional factors which transactivate autophagy genes...
May 2017: PLoS Genetics
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