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The Natural Course of Non-Alcoholic Fatty Liver Disease
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NAFLD and NASH in HCV Infection: Prevalence and Significance in Hepatic and Extrahepatic Manifestations

Department of Medical, Surgical, Neurological, Metabolic, and Geriatric Sciences, Second University of Naples, Naples 80100, Italy
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Author to whom correspondence should be addressed.
Academic Editors: Amedeo Lonardo and Giovanni Targher
Int. J. Mol. Sci. 2016, 17(6), 803; https://doi.org/10.3390/ijms17060803
Received: 14 March 2016 / Revised: 15 May 2016 / Accepted: 19 May 2016 / Published: 25 May 2016
(This article belongs to the Special Issue Non-Alcoholic Fatty Liver Disease Research 2016)
The aim of this paper is to review and up to date the prevalence of hepatitis C virus (HCV)-associated non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH) and their significance in both accelerating progression of HCV-related liver disease and development of HCV-associated extrahepatic diseases. The reported mean prevalence of HCV-related NAFLD was 55%, whereas NASH was reported in 4%–10% of cases. HCV genotype 3 directly induces fatty liver deposition, namely “viral steatosis” and it is associated with the highest prevalence and degree of severity, whereas, HCV non-3 genotype infection showed lower prevalence of steatosis, which is associated with metabolic factors and insulin resistance. The host’s genetic background predisposes him or her to the development of steatosis. HCV’s impairment of lipid and glucose metabolism causes fatty liver accumulation; this seems to be a viral strategy to optimize its life cycle. Irrespective of insulin resistance, HCV-associated NAFLD, in a degree-dependent manner, contributes towards accelerating the liver fibrosis progression and development of hepatocellular carcinoma by inducing liver inflammation and oxidative stress. Furthermore, NAFLD is associated with the presence of metabolic syndrome, type 2 diabetes, and atherosclerosis. In addition, HCV-related “metabolic steatosis” impairs the response rate to interferon-based treatment, whereas it seems that “viral steatosis” may harm the response rate to new oral direct antiviral agents. In conclusion, a high prevalence of NAFLD occurs in HCV infections, which is, at least in part, induced by the virus, and that NAFLD significantly impacts progression of the liver disease, therapeutic response, and some extrahepatic diseases. View Full-Text
Keywords: HCV-associated NAFLD; insulin resistance; liver fibrosis; HCC; metabolic syndrome; diabetes; atherosclerosis HCV-associated NAFLD; insulin resistance; liver fibrosis; HCC; metabolic syndrome; diabetes; atherosclerosis
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MDPI and ACS Style

Adinolfi, L.E.; Rinaldi, L.; Guerrera, B.; Restivo, L.; Marrone, A.; Giordano, M.; Zampino, R. NAFLD and NASH in HCV Infection: Prevalence and Significance in Hepatic and Extrahepatic Manifestations. Int. J. Mol. Sci. 2016, 17, 803. https://doi.org/10.3390/ijms17060803

AMA Style

Adinolfi LE, Rinaldi L, Guerrera B, Restivo L, Marrone A, Giordano M, Zampino R. NAFLD and NASH in HCV Infection: Prevalence and Significance in Hepatic and Extrahepatic Manifestations. International Journal of Molecular Sciences. 2016; 17(6):803. https://doi.org/10.3390/ijms17060803

Chicago/Turabian Style

Adinolfi, Luigi E.; Rinaldi, Luca; Guerrera, Barbara; Restivo, Luciano; Marrone, Aldo; Giordano, Mauro; Zampino, Rosa. 2016. "NAFLD and NASH in HCV Infection: Prevalence and Significance in Hepatic and Extrahepatic Manifestations" Int. J. Mol. Sci. 17, no. 6: 803. https://doi.org/10.3390/ijms17060803

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Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

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