Genotype 3 is associated with accelerated fibrosis progression in chronic hepatitis C

Bochud, Pierre‐Yves; Cai, Tao; Overbeck, Kathrin Stéphanie; Bochud, Murielle; Dufour, Jean‐François; Müllhaupt, Beat; Borovicka, Jan; Heim, Markus H.; Moradpour, Darius; Cerny, Andreas; Malinverni, Raffaele; Francioli, P.; Negro, Francesco

doi:10.1016/j.jhep.2009.05.016

Cited by 255 publications

(218 citation statements)

References 28 publications

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“…According to our data, patients with HCV genotype 3 have a faster disease progression, confirming other recent studies. 3,4 However, whether this association is directly mediated by the virus through the increased steatosis observed in patients with HCV genotype 3 or is a consequence of other external factors is still debated. 27,28 In our models, we included an interaction term between viral genotype and steatosis to account for the reasonable different influence of steatosis according to HCV genotype.…”

Section: Discussionmentioning

confidence: 99%

Genetic variation in the interleukin - 28B gene is not associated with fibrosis progression in patients with chronic hepatitis C and known date of infection

et al. 2011

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Polymorphisms in the interleukin-28B (IL28B) region are associated with spontaneous and treatment-induced viral clearance in hepatitis C virus (HCV) infection. Nevertheless, it is unknown whether genetic variation at the IL28B locus influences the natural history of chronic HCV infection. Thus, we asked whether an association between IL28B polymorphisms and liver fibrosis progression existed. We studied 247 consecutive patients with chronic HCV, an accurate estimate of the date of infection, and a liver biopsy performed before any treatment. No patient had a history of alcohol abuse or coinfection with other viruses. We assessed the role of rs8099917 and rs12979860 polymorphisms and the effect of host and environmental factors on fibrosis progression. Blood transfusion (75%) was the main modality of infection. Median age at infection was 21 years, and median interval between infection and liver biopsy was 25 years. One hundred twenty-nine patients (52%) were infected by HCV-1, 74 (30%) by HCV-2, 34 (14%) by HCV-3, and 10 (4%) by HCV-4. Bridging fibrosis/cirrhosis (Ishak !4) was detected in 24% of patients. Age at infection had a marked effect on fibrosis progression by both a linear model and Cox proportionalhazard regression (P < 2E-16). A 12.1% increase in the hazard of advanced fibrosis was estimated for each additional year at infection, suggesting that this was the major explanatory variable in this cohort. Male gender (P < 0.05), HCV genotype 3 (P < 0.001) and steatosis (P < 0.05) were also associated with faster fibrosis progression. Conversely, the two IL28B polymorphisms had no impact on fibrosis progression. Conclusion: In HCV patients with a known date of infection, IL28B genotype was not associated with fibrosis progression rate or with the risk of developing advanced liver fibrosis.

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Section: Discussionmentioning

confidence: 99%

Genetic variation in the interleukin - 28B gene is not associated with fibrosis progression in patients with chronic hepatitis C and known date of infection

et al. 2011

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“…In a Swiss study, genotype 3 HCV infection was associated with accelerated fibrosis progression compared to infection with other HCV genotypes. 151 Comparison of natural history of HCV infection in United Kingdom among persons originating from the Indian subcontinent with a group of White patients showed that Asian patients were more likely to be older, female, infected with genotype 3 and to not consume alcohol. The Asian patients had a significantly higher fibrosis score at the time of first biopsy (3.0 AE 2.3 vs. 1.8 AE 2.0, P < 0.001) and higher necro-inflammation and steatosis scores.…”

Section: Natural History Of Hcv In Indiamentioning

confidence: 99%

Consensus Statement of HCV Task Force of the Indian National Association for Study of the Liver (INASL). Part I: Status Report of HCV Infection in India

Puri

Anand

Saraswat

et al. 2014

Journal of Clinical and Experimental Hepatology

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Globally, around 150 million people are infected with hepatitis C virus (HCV). India contributes a large proportion of this HCV burden. The prevalence of HCV infection in India is estimated at between 0.5% and 1.5%. It is higher in the northeastern part, tribal populations and Punjab, areas which may represent HCV hotspots, and is lower in western and eastern parts of the country. The predominant modes of HCV transmission in India are blood transfusion and unsafe therapeutic injections. There is a need for large field studies to better understand HCV epidemiology and identify high-prevalence areas, and to identify and spread awareness about the modes of transmission of this infection in an attempt to prevent disease transmission. ( J CLIN EXP HEPATOL 2014;4:106-116)

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“…Our conclusions lean on the assumption that fibrosis rates are linear throughout the different stages, which is not confirmed [10,30]. This approximation, however, is of value for comparison between this and other studies.…”

Section: Discussionmentioning

confidence: 55%

Liver fibrosis progression at autopsy in injecting drug users infected by hepatitis C: A longitudinal long-term cohort study

Kielland

Delaveris

Rogde

et al. 2014

Journal of Hepatology

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Genotype 3 is associated with accelerated fibrosis progression in chronic hepatitis C

Cited by 255 publications

References 28 publications

Genetic variation in the interleukin - 28B gene is not associated with fibrosis progression in patients with chronic hepatitis C and known date of infection

Genetic variation in the interleukin - 28B gene is not associated with fibrosis progression in patients with chronic hepatitis C and known date of infection

Consensus Statement of HCV Task Force of the Indian National Association for Study of the Liver (INASL). Part I: Status Report of HCV Infection in India

Liver fibrosis progression at autopsy in injecting drug users infected by hepatitis C: A longitudinal long-term cohort study

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