Chapter 20 Effects of Hepatitis C Core Protein on Mitochondrial Electron Transport and Production of Reactive Oxygen Species

Campbell, Roosevelt V.; Yang, Yuanzheng; Wang, Ting; Rachamallu, Aparna; Li, Yanchun; Watowich, Stanley J.; Weinman, Steven A.

doi:10.1016/s0076-6879(08)04420-0

Cited by 11 publications

(6 citation statements)

References 24 publications

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“…ROS generation in rats of all groups was measured by the method of [4] using Varioskan fluorescent microplate reader. The method employs the measurement of ROS generation using the cell permeable fluorescent dye DCFH-DA (2′, 7-dichlorofluoresceindiacetate).…”

Section: Methodsmentioning

confidence: 99%

Naringenin accords hepatoprotection from streptozotocin induced diabetes in vivo by modulating mitochondrial dysfunction and apoptotic signaling cascade

Kapoor

Kakkar

2014

Toxicology Reports

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HighlightsStreptozotocin induced diabetes altered fasting blood glucose, body weight and carbohydrate metabolizing enzymes.Diabetes induced ROS, enhanced lipid peroxidation and protein carbonyl content while down-regulating antioxidants.Apoptotic proteins like AIF, Endo-G, Bax, Bcl-2, caspase-3 & 9 were significantly modulated during diabetes.Naringenin modulated the fasting glucose, carbohydrate metabolizing enzymes and antioxidant status of diabetic rats.Naringenin inhibited mitochondrial depolarization and up/down regulation of apoptotic/antiapoptotic proteins.

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Section: Methodsmentioning

confidence: 99%

Naringenin accords hepatoprotection from streptozotocin induced diabetes in vivo by modulating mitochondrial dysfunction and apoptotic signaling cascade

Kapoor

Kakkar

2014

Toxicology Reports

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“…Freshly isolated mitochondria were incubated with various concentrations of CaCl 2 at room temperature for 30 min in cytochrome c buffer (300 m m mannitol, 10 m m HEPES, 0.3 m m KH 2 PO 4 , pH 7.4). Exogenous core protein [35] at a concentration of 20 ng/mg mitochondrial protein was incubated with mitochondria along with Ca 2+ for 30 min when indicated. To the mixture, 50 μg/mL of proteinase K was then added to remove any cytochrome c that was released from the intermembrane space.…”

Section: Methodsmentioning

confidence: 99%

Role of Hepatitis C virus core protein in viral-induced mitochondrial dysfunction

Wang

Campbell

et al. 2009

Journal of Viral Hepatitis

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SUMMARY Hepatitis C virus (HCV) infection results in several changes in mitochondrial function including increased reactive oxygen species (ROS) production and greater sensitivity to oxidant, Ca2+ and cytokine-induced cell death. Prior studies in protein over-expression systems have shown that this effect can be induced by the core protein, but other viral proteins and replication events may contribute as well. To evaluate the specific role of core protein in the context of viral replication and infection, we compared mitochondrial sensitivity in Huh7-derived HCV replicon bearing cells with or without core protein expression with that of cells infected with the JFH1 virus strain. JFH1 infection increased hydrogen peroxide production and sensitized cells to oxidant-induced loss of mitochondrial membrane potential and cell death. An identical phenomenon occurred in genome-length replicons-bearing cells but not in cells bearing the subgenomic replicons lacking core protein. Both cell death and mitochondrial depolarization were Ca2+ dependent and could be prevented by Ca2+ chelation. The difference in the mitochondrial response of the two replicon systems could be demonstrated even in isolated mitochondria derived from the two cell lines with the ‘genome-length’ mitochondria displaying greater sensitivity to Ca2+-induced cytochrome c release. In vitro incubation of ‘subgenomic’ mitochondria with core protein increased oxidant sensitivity to a level similar to that of mitochondria derived from cells bearing genome-length replicons. These results indicate that increased mitochondrial ROS production and a reduced threshold for Ca2+ and ROS-induced permeability transition is a characteristic of HCV infection. This phenomenon is a direct consequence of core protein interactions with mitochondria and is present whenever core is expressed, either in infection, full-length replicon-bearing cells, or in over-expression systems.

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“…HSV1 downregulates the uptake of Ca 2+ by mitochondria along its lytic cycle, modulating virus replication (Lund and Ziola, 1985). Other viruses such as HCV target mitochondria, increasing Ca 2+ concentration (Li et al, 2007; Campbell et al, 2009). Among the HCV proteins known to interfere with Ca 2+ homeostasis, are the core protein, the NS5A, and the p7 protein (Gong et al, 2001; Griffin et al, 2004; Kalamvoki and Mavromara, 2004; Dionisio et al, 2009).…”

Section: Intracellular Calcium Homeostasis and Viral Infectionsmentioning

confidence: 99%

Virus Control of Cell Metabolism for Replication and Evasion of Host Immune Responses

Moreno-Altamirano

Kolstoe

Sánchez‐García

2019

Front. Cell. Infect. Microbiol.

105

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Over the last decade, there has been significant advances in the understanding of the cross-talk between metabolism and immune responses. It is now evident that immune cell effector function strongly depends on the metabolic pathway in which cells are engaged in at a particular point in time, the activation conditions, and the cell microenvironment. It is also clear that some metabolic intermediates have signaling as well as effector properties and, hence, topics such as immunometabolism, metabolic reprograming, and metabolic symbiosis (among others) have emerged. Viruses completely rely on their host's cell energy and molecular machinery to enter, multiply, and exit for a new round of infection. This review explores how viruses mimic, exploit or interfere with host cell metabolic pathways and how, in doing so, they may evade immune responses. It offers a brief outline of key metabolic pathways, mitochondrial function and metabolism-related signaling pathways, followed by examples of the mechanisms by which several viral proteins regulate host cell metabolic activity.

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Chapter 20 Effects of Hepatitis C Core Protein on Mitochondrial Electron Transport and Production of Reactive Oxygen Species

Cited by 11 publications

References 24 publications

Naringenin accords hepatoprotection from streptozotocin induced diabetes in vivo by modulating mitochondrial dysfunction and apoptotic signaling cascade

Naringenin accords hepatoprotection from streptozotocin induced diabetes in vivo by modulating mitochondrial dysfunction and apoptotic signaling cascade

Role of Hepatitis C virus core protein in viral-induced mitochondrial dysfunction

Virus Control of Cell Metabolism for Replication and Evasion of Host Immune Responses

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