Subsequent studies have implicated the hepatitis C virus (HCV) core protein in the pathogenesis of hepatic steatosis. Chronic HCV infection may also cause steatosis by impairing fatty acid oxidation. There is relationship between accumulation of fat into the liver and overweight and/or obesity. Another unexpected virus-host interaction is the HCV infection and diabetes. HCV encoded proteins might alter insulin signaling thus explaining impaired insulin sensitivity and the occurrence of glycaemic dysregulation. Some pieces of the puzzle are still not well known; e.g. the factors and the spectrum of disorders associated with insulin resistance, and whether the liver is a trigger or target of metabolic syndrome? In this review article clinical consequence of chronic HCV infection, diabetes mellitus and hepatic steatosis are discussed, as well as their possible effects on antiviral therapy.
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http://dx.doi.org/10.1556/OH.2011.29107 | DOI Listing |
Resistance-associated substitutions (RASs) are mutations within the hepatitis C (HCV) genome that may influence the likelihood of achieving a sustained virological response (SVR) with direct acting antiviral (DAA) treatment. Clinicians conduct RAS testing to adapt treatment regimens with the intent of improving the likelihood of cure. The Canadian Network Undertaking against Hepatitis C (CANUHC) prospective cohort consists of chronic HCV patients enrolled between 2015 and 2023 across 17 Canadian sites.
View Article and Find Full Text PDFInt J Biol Sci
January 2025
CAMS Key Laboratory of Antiviral Drug Research, Institute of Medicinal Biotechnology, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, 100050, China.
Although therapies based on direct-acting antivirals (DAAs) effectively eradicate hepatitis C virus (HCV) in patients, there is still a high risk of liver fibrosis even after a sustained virological response. Therefore, it is of great clinical importance to understand the mechanism of potential factors that promote liver fibrosis after virological cure by treatment with DAAs. Here, we found that tubulointerstitial nephritis antigen-like 1 (TINAGL1) is significantly increased in HCV-infected hepatocytes and in the liver of patients with liver fibrosis, and that higher TINAGL1 expression persists in HCV-eradicated hepatocytes after treatment with DAAs.
View Article and Find Full Text PDFCureus
December 2024
Diagnostic Radiology, Bolan Medical College Quetta, Quetta, PAK.
Introduction Although metabolic dysfunction-associated fatty liver disease (MAFLD) is becoming more common in individuals with hepatocellular carcinoma (HCC), it is still unknown how this condition relates to postoperative complications of HCC. While hepatitis B/C virus (HBV/HCV) infection and alcohol use are primary risk factors, MAFLD has emerged as a significant contributor to HCC incidence. Understanding the prognostic impact of MAFLD on HCC outcomes, particularly post-radical resection, is essential.
View Article and Find Full Text PDFBMC Gastroenterol
January 2025
Department of Community Health Sciences, College of Applied Medical Sciences, King Saud University, Riyadh, 11433, Saudi Arabia.
Background: Viral hepatitis is the major contributor to liver cirrhosis and hepatocellular carcinoma (HCC). Studies indicated that the co-infection of hepatitis C and hepatitis B virus also prompts liver damage progression. Therefore, in the present study, the prevalence of HCV-HBV co-infection and the impact of HCV-HBV co-infection on the progression of liver damage was evaluated amongst the HCV-infected patients in Pakistan.
View Article and Find Full Text PDFTransplant Proc
January 2025
Hepatobiliary Surgery and Liver Transplantation Unit, Cruces University Hospital, Bilbao, Spain. Electronic address:
Background: The progressive increase in the prevalence of morbid obesity (MO) in the general population is a pressing issue. This rise in MO has also been observed in patients with liver disease who are candidates for liver transplantation (LT).
Methods: A retrospective study of a single-center series was conducted to analyze the impact of MO on morbidity, mortality, and patient survival after LT.
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