Influence of Chronic Alcohol Abuse on Hepatitis C Virus Replication

Anand, B S; Velez, Maria

doi:10.1159/000051390

Cited by 25 publications

(21 citation statements)

References 22 publications

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“…A recent report, however, suggests that alcohol intake does not acutely increase HCV RNA serum levels. 25 The mode of infection did not seem to be a factor in the progressive nature of this viral infection in our patient population. We were unable to show a difference in the incidence of cirrhosis or decompensated liver disease in patients infected with HCV by blood products or exposure to intravenous drugs when patients were stratified as to whether they did or did not drink.…”

Section: Discussionmentioning

confidence: 54%

Impact of alcohol on the histological and clinical progression of Hepatitis C infection

et al. 1998

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In patients infected with the hepatitis C virus (HCV), 20% to 30% will progress to cirrhosis in over two to three decades. Viral and host factors that are important in the clinical and histologic progression of HCV infection are not entirely certain. It has been suggested that liver disease is worse in alcoholics infected with HCV. In the present retrospective study, we examined the effect of moderate alcohol intake on the histologic and clinical progression of HCV infection and assessed whether other variables such as gender, length of exposure, mode of exposure, HCV RNA levels, and ferritin levels also independently impacted disease progression. Liver biopsies were analyzed for the degree of fibrosis, presence of cirrhosis, and histologic activity by using the Histologic Activity Index of Knodell. Patients were divided into two groups based on whether their alcohol intake was significant or not significant. Significant alcohol intake was defined as G40 g alcohol/day in women and G60 g of alcohol/day in men for G5 years. Groups were further divided based on the decades of exposure to HCV. There was no difference in the age or length of exposure to HCV in the alcohol and the alcoholfree group. HCV RNA serum levels, ferritin levels, and viral genotypes were similar in both groups. There was a two-to threefold greater risk of liver cirrhosis and decompensated liver disease in the alcohol group. Also, the rate to which subjects developed cirrhosis was faster in the alcohol group with 58% being cirrhotic by the second decade as opposed to 10% being cirrhotic in the nonalcohol group by the second decade. The histologic and clinical acceleration of liver disease was independent of the mode of exposure or sex. In summary, alcohol intake is an independent risk factor in the clinical and histologic progression of HCV infection. (HEPATOLOGY 1998;28:805-809.)In the United States 3 to 4 million people are infected with HCV. HCV infection is an indolent disease with patients rarely having clinical symptoms until cirrhosis develops. Ten to thirty percent of patients infected with HCV will develop cirrhosis over a 20 to 30 year period, and 1% to 5% will develop hepatocellular carcinoma. [1][2][3][4] Host and viral factors that are important in enhancing the progression to cirrhosis are not entirely clear. 5 Proposed contributory factors include viral genotype, circulating viral load, duration of infection, mode of infection, iron load, gender, and alcohol consumption. [1][2][3][4][5] It is recognized that 5% to 25% of chronic alcoholics with liver disease have a positive HCV antibody test. 6-12 Also, a number of studies have suggested that patients with alcoholic liver disease who are infected with the HCV have more impaired biochemical function and a greater chance of developing cirrhosis. [6][7][8][9][10][11][12] Alcohol intake has also been implicated as an independent risk factor in the progression of HCV, 13 although its overall effect on both the histologic and clinical progression of liver disease in patients chronicall...

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Section: Discussionmentioning

confidence: 54%

Impact of alcohol on the histological and clinical progression of Hepatitis C infection

et al. 1998

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“…The use of alcohol has been found to be associated with immune control of HCV and to affect HCV replication and/or viral clearance. This final effect may have an impact on the evolution of HCV quasispecies, presumably through its effects on the immune system (7,8).…”

Section: Introductionmentioning

confidence: 99%

Molecular Mechanisms Involved in the Interaction Effects of Alcohol and Hepatitis C Virus in Liver Cirrhosis

Mas

Fassnacht

Archer

et al. 2010

Mol Med

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The mechanisms by which alcohol consumption accelerates liver disease in patients with chronic hepatitis C virus (HCV) are not well understood. To identify the characteristics of molecular pathways affected by alcohol in HCV patients, we fit probe-set level linear models that included the additive effects as well as the interaction between alcohol and HCV. The study included liver tissue samples from 78 patients, 23 (29.5%) with HCV-cirrhosis, 13 (16.7%) with alcohol-cirrhosis, 23 (29.5%) with HCV/alcohol cirrhosis and 19 (24.4%) with no liver disease (no HCV/no alcohol group). We performed gene-expression profiling by using microarrays. Probe-set expression summaries were calculated by using the robust multiarray average. Probe-set level linear models were fit where probe-set expression was modeled by HCV status, alcohol status, and the interaction between HCV and alcohol. We found that 2172 probe sets (1895 genes) were differentially expressed between HCV cirrhosis versus alcoholic cirrhosis groups. Genes involved in the virus response and the immune response were the more important upregulated genes in HCV cirrhosis. Genes involved in apoptosis regulation were also overexpressed in HCV cirrhosis. Genes of the cytochrome P450 superfamily of enzymes were upregulated in alcoholic cirrhosis, and 1230 probe sets (1051 genes) had a significant interaction estimate. Cell death and cellular growth and proliferation were affected by the interaction between HCV and alcohol. Immune response and response to the virus genes were downregulated in HCV-alcohol interaction (interaction term alcohol*HCV). Alcohol*HCV in the cirrhotic tissues resulted in a strong negative regulation of the apoptosis pattern with concomitant positive regulation of cellular division and proliferation.

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“…In the United States, about half of the causes of death in liver cirrhosis is alcohol abuse or alcoholism, a situation which is quite different from Japan, where 80-90% of cause of cirrhosis is chronic viral infection. Although, many ALD patients were found to have chronic hepatitis C after discovery of hepatitis C virus (HCV), alcohol intake is an exacerbating factor of chronic hepatitis C [1], and HCV infection is an exacerbating factor of ALD [2]. Eradication of HCV by interferon therapy may result in an increase in the proportion of ALD among chronic liver diseases in Japan in the future.…”

Section: Introductionmentioning

confidence: 99%