Liver steatosis in hepatitis C patients

Abstract

would affect HCV patients who are also obese or diabetics. In fact, several genotypes exert metabolic effects which overlap with some of those observed in the metabolic syndrome. In this review we will analyse the pathogenic pathways involved in the development of steatosis in HCV patients. Several cytokines and adipokines also become activated and are involved in "pure" steatosic effects, in addition to inflammation. They are probably responsible for the evolution of simple steatosis to steatohepatitis, making it difficult to explain why such alterations only affect a proportion of steatosic patients. Core tip: Chronic hepatitis C virus (HCV) infection can lead to steatosis and steatohepatitis. Increased liver triglyceride synthesis is mediated by several transcription factors such as sterol regulatory elementbinding protein (SREBP) whose expression is enhanced, in turn, by HCV core protein. Chronic HCV infection is also associated with insulin resistance that seems to be selective because although it activates systemic lipolysis, it increases triglyceride synthesis within the liver. This is due to the stimulatory effect of insulin on SREBP. It remains to be answered why not all patients with HCV infection and steatosis develop steatohepatitis despite early cytokine activation and metabolic derangements. AbstractThere is controversy regarding some aspects of hepatitis C virus (HCV) infection-associated liver steatosis, and their relationship with body fat stores. It has classically been found that HCV, especially genotype 3, exerts direct metabolic effects which lead to liver steatosis. This supports the existence of a so called viral steatosis and a metabolic steatosis, which REVIEWSubmit a

Utility of shear‐wave elastography to differentiate low from advanced degrees of liver fibrosis in patients with hepatitis C virus infection of native and transplant livers

“…There is an increased prevalence of steatosis in patients with chronic hepatitis C, but it is not firmly established whether fat deposition is directly due to the virus itself, or whether it is secondary to liver dysfunction caused by chronic infection. [31][32][33] In this study, as was previously reported, 29 there was no demonstrable effect of the presence of fat on SWE liver parenchymal stiffness values in either the native or the transplanted livers. We speculate that the speed of the shear waves in fat is similar to that in normal liver tissue.…”

CD2‐Associated Protein Contributes to Hepatitis C, Virus Propagation and Steatosis by Disrupting Insulin Signaling

“…Liver pathologies, such as steatosis, are affected by many factors . Here, we provide insights into the propagation of HCV and steatosis caused by chronic HCV infection.…”

Target delivery of small interfering RNAs with vitamin E-coupled nanoparticles for treating hepatitis C

“…Hepatitis C virus (HCV) is a major cause of chronic liver disease and affects over 185 million individuals worldwide 1 . Persistent HCV infection is a leading cause of chronic hepatitis, liver cirrhosis, and even hepatocellular carcinoma 2 3 . Although HCV infections can be partially combatted by the new treatment regimens with direct-acting antiviral drugs (DAAs), the high specificity of DAAs against their viral targets might result in emergence of antiviral resistance, and even these regimens are costly which might also lead to a restricting societal benefit 4 .…”