Oxidized low-density lipoprotein is associated with viral load and disease activity in patients with chronic hepatitis C

Nakhjavani, Manouchehr; Mashayekh, Arshideh; Khalilzadeh, Omid; Asgarani, Firouzeh; Morteza, Afsaneh; Omidi, Mohammad; Froutan, Hossein

doi:10.1016/j.clinre.2010.11.001

Cited by 17 publications

(14 citation statements)

References 34 publications

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“…Given that in vivo HCV viral load varies between and within individuals over a wide range and is likely influenced by a multitude of variables, this is not very surprising. Differently from our data, a recent study reported on a positive correlation between oxLDL and HCV viral load 39 ; however, it appears that this hinged strongly on a small number of outliers with very high oxLDL levels and viral load, whereas the majority of the population was similar to our cohort in showing a weak negative correlation that likely falls short of statistical significance.…”

Section: Discussioncontrasting

confidence: 99%

Characterization of the inhibition of hepatitis C virus entry by In vitro –generated and patient-derived oxidized low-density lipoprotein

et al. 2013

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Oxidized low-density lipoprotein (oxLDL) has been reported as an inhibitor of hepatitis C virus (HCV) cell entry, making it the only known component of human lipid metabolism with an antiviral effect on HCV. However, several questions remain open, including its effect on full-length cell-culture-grown HCV (HCVcc) of different genotypes or on other steps of the viral replication cycle, its mechanism of action, and whether endogenous oxLDL shares the anti-HCV properties of in vitro-generated oxLDL. We combined molecular virology tools with oxLDL serum measurements in different patient cohorts to address these questions. We found that oxLDL inhibits HCVcc at least as potently as HCV pseudoparticles. There was moderate variation between genotypes, with genotype 4 appearing the most oxLDL sensitive. Intracellular RNA replication and assembly and release of new particles were unaffected. HCV particles entering target cells lost oxLDL sensitivity with time kinetics parallel to anti-SR-BI (scavenger receptor class B type I), but significantly earlier than anti-CD81, suggesting that oxLDL acts by perturbing interaction between HCV and SR-BI. Finally, in chronically HCV-infected individuals, endogenous serum oxLDL levels did not correlate with viral load, but in HCV-negative sera, high endogenous oxLDL had a negative effect on HCV infectivity in vitro. Conclusion: oxLDL is a potent pangenotype HCV entry inhibitor that maintains its activity in the context of human serum and targets an early step of HCV entry. (HEPATOLOGY 2013;57:1716-1724 C hronic hepatitis C virus (HCV) infection affects an estimated 160 million people worldwide. 1 Chronic HCV is a frequent cause of end-stageliver diseases (ESLDs) and hepatocellular carcinoma as well as a common indication for liver transplantation (LT). Treatment remains problematic because of side effects and high cost. A particular problem is graft reinfection that occurs immediately after LT for HCVassociated ESLD and often leads to transplant hepatitis and graft loss. 2 The HCV replication cycle is intricately linked to host lipid metabolism. 3 The production of infectious viral particles is dependent on the cellular very-lowdensity lipoprotein (VLDL) assembly machinery, and

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Section: Discussioncontrasting

confidence: 99%

Characterization of the inhibition of hepatitis C virus entry by In vitro –generated and patient-derived oxidized low-density lipoprotein

et al. 2013

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“…Nakhjavani and colleagues also confirmed significant higher level of oxLDL in patients with CH-C than in NHCs [33]. Increased serum oxLDL levels seemed to be derived from oxidative stress by persistent HCV infection.…”

Section: Discussionmentioning

confidence: 86%

Investigation of the factors associated with circulating soluble CD36 levels in patients with HCV-related chronic liver disease

Himoto

Tani

Miyoshi

et al. 2013

Diabetol Metab Syndr

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BackgroundCD36, a class B scavenger receptor, participates in the pathogenesis of metabolic dysregulation such as insulin resistance, hepatic steatosis, and atherosclerosis. Persistent hepatitis C virus (HCV) infection often evokes these metabolic abnormalities. The primary purpose of this study was to investigate the role of CD36 in the pathogenesis of insulin resistance and hepatic steatosis caused by chronic HCV infection.MethodsForty-five patients with HCV-related chronic liver disease (CLD-C) were enrolled in this study. CD36 expression in the liver specimen was examined by an immunohistochemical procedure. The concentrations of circulating soluble form of CD36 (sCD36) and oxLDL were determined by the enzyme-linked innunosorbent assay. Insulin resistance was estimated by the values of HOMA-IR.ResultsModerate to extensive hepatic CD36 expression was observed in the sinusoids of all enrolled CLD-C patients. CD36-positive sinusoids appeared to be identical to Kupffer cells. The severity of CD36 expression in the hepatic sinusoids was significantly correlated with the sCD36 level in sera of patients with CLD-C. The serum sCD36 levels were significantly correlated with body mass index and serum oxLDL levels in those patients. However, the serum sCD36 concentrations were independent of the values of HOMA-IR and the severity of hepatic steatosis.ConclusionsThese data suggest that the serum sCD36 levels reflect the severity of CD36 expression on the Kupffer cells in patients with CLD-C, and that the serum sCD36 levels were associated with obesity, although the levels were independent of insulin resistance and hepatic steatosis in those patients.

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“…Nakhjavani et al 34 have reported that oxidative stress and lipid peroxidation play a major role in liver injury in chronic HCV infection and that viral load correlated with the serum level of oxidized LDL.…”

Section: Discussionmentioning

confidence: 99%

RANTES, TNF-α, Oxidative Stress, and Hematological Abnormalities in Hepatitis C Virus Infection

Tawadrous

Aziz²,

Amin³

et al. 2012

Journal of Investigative Medicine

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Oxidized low-density lipoprotein is associated with viral load and disease activity in patients with chronic hepatitis C

Cited by 17 publications

References 34 publications

Characterization of the inhibition of hepatitis C virus entry by In vitro –generated and patient-derived oxidized low-density lipoprotein

Characterization of the inhibition of hepatitis C virus entry by In vitro –generated and patient-derived oxidized low-density lipoprotein

Investigation of the factors associated with circulating soluble CD36 levels in patients with HCV-related chronic liver disease

RANTES, TNF-α, Oxidative Stress, and Hematological Abnormalities in Hepatitis C Virus Infection

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