Hepatitis C virus–apolipoprotein interactions: molecular mechanisms and clinical impact

Crouchet, Émilie; Baumert, Thomas F.; Schuster, Catherine

doi:10.1080/14789450.2017.1344102

Cited by 19 publications

(19 citation statements)

References 124 publications

(186 reference statements)

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“…The formation of HCV lipoviral particles (LVP) occurs within the endoplasmic reticulum at interfaces between lipid droplets and is closely intertwined with lipid and lipoprotein metabolism [40]. As such, apolipoproteins are essential regulators of lipid metabolism and play an important role in the HCV life cycle [41]. apoB forms the protein backbone for the formation of TG lipoproteins including chylomicrons and VLDL as well as post-hydrolysis LDL.…”

Section: Discussionmentioning

confidence: 99%

“…apoB forms the protein backbone for the formation of TG lipoproteins including chylomicrons and VLDL as well as post-hydrolysis LDL. In contrast to apoB, other apolipoproteins including apoA1, apoC2, apoC3, and apoE are easily disassociated and can be exchanged between different classes of lipoproteins and the surface of HCV LVPs [41]. apoE association with HCV lipoviral particles enhances infectivity [13,42,43,44,45].…”

Section: Discussionmentioning

confidence: 99%

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Hepatitis C Direct Acting Antivirals and Ribavirin Modify Lipid but not Glucose Parameters

Doyle

Galanakis

Mulvihill

et al. 2019

Cells

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Chronic hepatitis C (HCV) infection perturbs lipid and glucose metabolism. The influenceof direct acting antiviral (DAA) treatment and ribavirin on these measures was evaluated.Furthermore, the effect of HCV cure on these parameters was assessed. Participants were allocatedto one of three 12-week treatment groups: non-cirrhotic genotype 1aparitaprevir/ritonavir/ombitasvir/dasabuvir (PrOD) plus ribavirin; non-cirrhotic 1b-PrOD;compensated cirrhotic 1a or 1b-PrOD plus ribavirin. Fasting insulin, glucose, lipid andapolipoprotein measures were assessed at baseline, Treatment Weeks 4 and 12, and 12 and 24 weekspost-dosing. Twenty-three of 24 participants achieved SVR (PP= 23/24, 96% SVR). Overall, totalcholesterol, low-density lipoprotein cholesterol (LDL-C), and triglyceride levels all increased intreatment and post-dosing. However, LDL-C levels decreased during treatment in ribavirinrecipients. Fasting glucose, insulin, and HOMA-IR were unchanged during treatment and 12 weekspost-treatment. By 12 weeks post-treatment, controlled attenuation parameter (CAP) scores, ameasure of steatosis, increased from baseline (mean 30.3 ± 63.5, p = 0.05). This regimen was safe andhighly effective and did not influence glucose metabolism. Ribavirin exposure may mitigate someon-treatment lipid changes. Further mechanistic studies are needed to understand how ribavirinimpacts lipid pathways, as there could be therapeutic implications. The metabolic pathophysiologyof increased CAP score with HCV treatment requires explanation.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Hepatitis C Direct Acting Antivirals and Ribavirin Modify Lipid but not Glucose Parameters

Doyle

Galanakis

Mulvihill

et al. 2019

Cells

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“…Characterization of HCV particles produced in cell culture (HCVcc) has confirmed these properties ( 16 – 18 ). Interactions of HCV particles with lipoprotein components play a critical role in the viral life cycle and contribute to viral persistence and development of chronic liver diseases ( 19 ).…”

Section: The Functional Role Of Apolipoproteins In the Hcv Life Cyclementioning

confidence: 99%

Hepatitis C Virus (HCV)–Apolipoprotein Interactions and Immune Evasion and Their Impact on HCV Vaccine Design

et al. 2018

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With more than 71 million people chronically infected, hepatitis C virus (HCV) is one of the leading causes of liver disease and hepatocellular carcinoma. While efficient antiviral therapies have entered clinical standard of care, the development of a protective vaccine is still elusive. Recent studies have shown that the HCV life cycle is closely linked to lipid metabolism. HCV virions associate with hepatocyte-derived lipoproteins to form infectious hybrid particles that have been termed lipo-viro-particles. The close association with lipoproteins is not only critical for virus entry and assembly but also plays an important role during viral pathogenesis and for viral evasion from neutralizing antibodies. In this review, we summarize recent findings on the functional role of apolipoproteins for HCV entry and assembly. Furthermore, we highlight the impact of HCV–apolipoprotein interactions for evasion from neutralizing antibodies and discuss the consequences for antiviral therapy and vaccine design. Understanding these interactions offers novel strategies for the development of an urgently needed protective vaccine.

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“…Apolipoproteins were also found in our results. Apolipoproteins play an important role in hepatitis C virus (HCV) pathogenesis, including in viral attachment, entry, and assembly [41]. They may not only participate in NNV entry, but also involve other NNV morphogenesis stages.…”

Section: Discussionmentioning

confidence: 99%

Screening for the Proteins That Can Interact with Grouper Nervous Necrosis Virus Capsid Protein

Huang

Hsiao

Wang

et al. 2020

Viruses

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Nervous necrosis virus (NNV) can infect many species of fish and has an 80–100% mortality rate. NNV capsid protein (NNVCP) is the only structural protein of NNV, but there are few studies on the protein–protein interaction between NNVCP and the host cell. To investigate NNV morphogenesis, native NNV capsid protein (NNVCP) was used to screen for protein–protein interactions in this study. The results identified that 49 grouper optic nerve proteins can interact with NNVCP and may function as putative receptor or co-receptor, cytoskeleton, glucose metabolism and ATP generation, immunity, mitochondrial ion regulation, and ribosomal proteins. Creatine kinase B-type (CKB) is one of those 49 optic nerve proteins. CKB, a kind of enzyme of ATP generation, was confirmed to interact with NNVCP by far-Western blot and showed to colocalize with NNVCP in GF-1 cells. Compared to the control, the expression of CKB was significantly induced in the brain and eyes infected with NNV. Moreover, the amount of replication of NNV is relatively high in cells expressing CKB. In addition to providing the database of proteins that can interact with NNVCP for subsequent analysis, the results of this research also verified that CKB plays an important role in the morphogenesis of NNV.

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Hepatitis C virus–apolipoprotein interactions: molecular mechanisms and clinical impact

Cited by 19 publications

References 124 publications

Hepatitis C Direct Acting Antivirals and Ribavirin Modify Lipid but not Glucose Parameters

Hepatitis C Direct Acting Antivirals and Ribavirin Modify Lipid but not Glucose Parameters

Hepatitis C Virus (HCV)–Apolipoprotein Interactions and Immune Evasion and Their Impact on HCV Vaccine Design

Screening for the Proteins That Can Interact with Grouper Nervous Necrosis Virus Capsid Protein

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