Steatosis accelerates fibrosis development over time in hepatitis C virus genotype 3 infected patients

Westin, Johan; Nordlinder, Hans; Lagging, Martin; Norkrans, Gunnar; Wejstål, Rune

doi:10.1016/s0168-8278(02)80488-3

Cited by 77 publications

(114 citation statements)

References 0 publications

Supporting

Mentioning

104

Contrasting

Unclassified

Order By: Relevance

“…There is some controversy with regard to the influence of steatosis on the progression of fibrosis [1,3]. Some investigators suggest that steatosis accelerates fibrosis only in genotype 3-infected patients [7,29,30], whereas others suggest that there is an association in patients infected with genotype 1 [5,31]. An analysis using paired liver biopsies revealed that steatosis was the only independent factor predictive of progression of fibrosis [32].…”

Section: Discussionmentioning

confidence: 99%

Steatosis and hepatic expression of genes regulating lipid metabolism in Japanese patients infected with hepatitis C virus

et al. 2009

View full text Add to dashboard Cite

show abstract

Section: Discussionmentioning

confidence: 99%

Steatosis and hepatic expression of genes regulating lipid metabolism in Japanese patients infected with hepatitis C virus

et al. 2009

View full text Add to dashboard Cite

show abstract

“…Conversely, in a study with a total of 1915 CHB patients in China, of which 260 (14 %) patients presented with steatosis, no significant difference in viral factors including the HBeAg and HBV DNA was found between those with and without steatosis [19], but still the group of steatosis patients demonstrated a relatively reduced histologic severity. Till now, it has been widely recognized that the presence of steatosis can accelerate the fibrosis progression in CHC individuals [114]. Nevertheless, whether steatosis is associated with the severity of fibrosis in CHB patients remains to be determined.…”

Section: Effects Of Nafld On the Virology And Fibrosis Progression Ofmentioning

confidence: 99%

Interactions of Hepatitis B Virus Infection with Nonalcoholic Fatty Liver Disease: Possible Mechanisms and Clinical Impact

et al. 2015

View full text Add to dashboard Cite

Hepatitis B virus (HBV) infection is a major etiology of chronic liver disease worldwide. In the past decade, nonalcoholic fatty liver disease (NAFLD) has emerged as a common liver disorder in general population. Accordingly, the patient number of chronic hepatitis B (CHB) concomitant with NAFLD grows rapidly. The present article reviewed the recent studies aiming to explore the relationship between CHB and NAFLD from different aspects, including the relevant pathogenesis of CHB and NAFLD, the intracellular molecular mechanisms overlaying HBV infection and hepatic steatosis, and the observational studies with animal models and clinical cohorts for analyzing the coincidence of the two diseases. It is concluded that although numerous cross-links have been suggested between the molecular pathways in HBV infection and NAFLD pathogenesis, regarding whether HBV infection can substantially interfere with the occurrence of NAFLD or vice versa in the patients, there is still far from a conclusive agreement.

show abstract

“…All HCV genotypes share a common genome organization and replication scheme. Despite the genome organization there is evidence of biological differences (e.g., low response to IFN-based therapies for genotype 1 viruses and a lower frequency of long-term persistent infection with genotype 3 virus) [84][85][86]. However, the different clinical behavior of HCV infection, its chronicity, and the severity of the liver damage are associated with the degree of liver steatosis [86,87] that contributes to HSC activation leading to fibrogenesis [87].…”

Section: Fibrosis and Hcvmentioning

confidence: 99%

“…Despite the genome organization there is evidence of biological differences (e.g., low response to IFN-based therapies for genotype 1 viruses and a lower frequency of long-term persistent infection with genotype 3 virus) [84][85][86]. However, the different clinical behavior of HCV infection, its chronicity, and the severity of the liver damage are associated with the degree of liver steatosis [86,87] that contributes to HSC activation leading to fibrogenesis [87]. Different vigor of the anti-viral cell-mediated immune response [88] and the core, envelope (E1-E2), or non-structural proteins (NSPs) encoded in the HCV genome may prime CD4 + T cells by dendritic cells expressing hepatitis C virus and may influence stimulation of lymphocytes to produce cytokines and to contribute to viral persistence [89][90][91].…”

Section: Fibrosis and Hcvmentioning

confidence: 99%

Inflammation and Repair in Viral Hepatitis C

et al. 2007

View full text Add to dashboard Cite

Hepatitis C viral infection (HCV) results in liver damage leading to inflammation and fibrosis of the liver and increasing rates of hepatic decompensation and hepatocellular carcinoma (HCC). However, the host's immune response and viral determinants of liver disease progression are poorly understood. This review will address the determinants of liver injury in chronic HCV infection and the risk factors leading to rapid disease progression. We aim to better understand the factors that distinguish a relatively benign course of HCV from one with progression to cirrhosis. We will accomplish this task by discussion of three topics: (1) the role of cytokines in the adaptive immune response against the HCV infection; (2) the progression of fibrosis; and (3) the risk factors of co-morbidity with alcohol and human immunodeficiency virus (HIV) in HCV-infected individuals. Despite recent improvements in treating HCV infection using pegylated interferon alpha (PEGIFN-alpha) and ribavirin, about half of individuals infected with some genotypes, for example genotypes 1 and 4, will not respond to treatment or cannot be treated because of contraindications. This review will also aim to describe the importance of IFN-alpha-based therapies in HCV infection, ways of monitoring them, and associated complications.

show abstract

Steatosis accelerates fibrosis development over time in hepatitis C virus genotype 3 infected patients

Cited by 77 publications

References 0 publications

Steatosis and hepatic expression of genes regulating lipid metabolism in Japanese patients infected with hepatitis C virus

Steatosis and hepatic expression of genes regulating lipid metabolism in Japanese patients infected with hepatitis C virus

Interactions of Hepatitis B Virus Infection with Nonalcoholic Fatty Liver Disease: Possible Mechanisms and Clinical Impact

Inflammation and Repair in Viral Hepatitis C

Contact Info

Product

Resources

About