Correspondence. Intranuclear Particles in Non-A, Non-B Hepatitis

doi:10.1002/hep.1840040342

Cited by 3 publications

(1 citation statement)

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“…Histological examinations show that up to 50% of these patients have variable degrees of hepatic steatosis [4], even in the absence of other possible steatogenic factors, like alcohol, drugs or metabolic syndrome [5]. Early electron microscopy studies conducted in experimentally infected chimps or parenterally infected humans with non A and non B hepatitis showed presence of abnormal cytoplasmic vesicular changes [6]. In hepatitis C Virus (HCV) infected patients liver steatosis is mainly macrovesicular [7] and is located in the periportal area rather than in the centrilobular area [8], in contrast to what is observed in non-alcoholic fatty liver disease (NAFLD) and in alcoholic liver disease.…”

Section: Introductionmentioning

confidence: 99%

Hepatic steatosis in hepatitis C is a storage disease due to HCV interaction with microsomal triglyceride transfer protein (MTP)

et al. 2010

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Liver steatosis is a frequent histological feature in patients chronically infected with hepatitis C virus (HCV). The relationship between HCV and hepatic steatosis seems to be the result of both epigenetic and genetic factors. In vivo and in vitro studies have shown that HCV can alter intrahepatic lipid metabolism by affecting lipid synthesis, oxidative stress, lipid peroxidation, insulin resistance and the assembly and secretion of VLDL. Many studies suggest that HCV-related steatosis might be the result of a direct interaction between the virus and MTP. It has been demonstrated that MTP is critical for the secretion of HCV particles and that inhibition of its lipid transfer activity reduces HCV production. However, higher degrees of hepatic steatosis were found in chronic hepatitis C patients carrying the T allele of MTP -493G/T polymorphism that seems to be associated with increased MTP transcription. We propose here that liver steatosis in hepatitis C could be a storage disease induced by the effects of the virus and of its proteins on the intracellular lipid machinery and on MTP. Available data support the hypothesis that HCV may modulate MTP expression and activity through a number of mechanisms such as inhibition of its activity and transcriptional control. Initial up regulation could favour propagation of HCV while down regulation in chronic phase could cause impairment of triglyceride secretion and excessive lipid accumulation, with abnormal lipid droplets facilitating the "storage" of virus particles for persistent infection.

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Section: Introductionmentioning

confidence: 99%

Hepatic steatosis in hepatitis C is a storage disease due to HCV interaction with microsomal triglyceride transfer protein (MTP)

et al. 2010

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Ultrastructural approach to liver pathology

Bonvicini

R²

1990

Ultrastructure of the Extraparietal Glands of the Digestive Tract

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An Ultrastructural Study of Six Cases of Chronic Active C Hepatitis. A Comparison with Chronic Active B Hepatitis

Balercia

Accordini

Piramo

et al. 1993

Ultrastructural Pathology

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Liver biopsies from six patients affected by chronic active hepatitis (CAH) induced by hepatitis C virus (HCV) have been investigated ultrastructurally and their features compared with those of five cases of CAH induced by hepatitis B virus (HBV). Clusters of deeply packed nuclear inclusions (18 to 22 nm in diameter) were found in patients with HCV-CAH. They were irregularly round and ill-delimited. These inclusions were distinct from the regular round and well-delimited nuclear inclusions associated with HBV. HCV-associated nuclear inclusions were similar to a peculiar type of intranuclear particle described in non-A, non-B hepatitis before the HCV disease had been recognized as a distinct entity. These inclusions have never been hitherto reported in infections caused by HBV or other known hepatotropic viruses. Together, these data suggest that the occurrence of these inclusions can be related to HCV activity in hepatocytes. Changes in the microarchitecture of the liver cell and its microenvironment were similar in HCV- and HBV-CAH. They were heterogeneous in different cases and did not display a clear correlation with the severity of the disease.

show abstract

Correspondence. Intranuclear Particles in Non-A, Non-B Hepatitis

Cited by 3 publications

References 19 publications

Hepatic steatosis in hepatitis C is a storage disease due to HCV interaction with microsomal triglyceride transfer protein (MTP)

Hepatic steatosis in hepatitis C is a storage disease due to HCV interaction with microsomal triglyceride transfer protein (MTP)

Ultrastructural approach to liver pathology

An Ultrastructural Study of Six Cases of Chronic Active C Hepatitis. A Comparison with Chronic Active B Hepatitis

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