The natural course of hepatitis C virus infection after 22 years in a unique homogenous cohort: spontaneous viral clearance and chronic HCV infection

Barrett, Sharon; Goh, J; Coughlan, Barbara; Ryan, Eleanor; Stewart, Stephen; Cockram, A; O'Keane, J C; Crowe, J.

doi:10.1136/gut.49.3.423

Cited by 141 publications

(121 citation statements)

References 51 publications

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“…The median fibrosis progression rate of 0.07 per year observed in this cohort was similar to or lower than reported in other studies of patients with chronic HCV-infection [16][17][18][19][20], but the progression rate was higher than in studies of young females who contracted an HCVinfection accidentally as a result of infected anti-D immunoglobulin in Ireland and Germany [5,21]. In a meta-analysis of the stage-specific fibrosis progression rate in different populations of HCV-patients, the mean progression rate among the IDUs were: F0-F1 0.116, F1-F2 0.085, F2-F3 0.085 and F3-F4 0.130 [20].…”

Section: Discussionsupporting

confidence: 81%

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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Section: Discussionsupporting

confidence: 81%

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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“…In the Irish anti-D cohort, a 22-year follow-up study also showed mild fibrosis progression in affected women. 9 Third, we could not reliably evaluate alcohol consumption in our patients over this long observation period. However, we observed only a minority of patients with excessive alcohol consumption in our 25-year follow-up study.…”

Section: Discussionmentioning

confidence: 93%

“…8 Therefore the well-documented iatrogenic singlesource HCV outbreaks in recipients of HCVcontaminated anti-D immunoglobulin (Ig) in Ireland (1977Ireland ( -1978 and Germany (1978Germany ( -1979 provided valuable insight into the acute and chronic course of HCV infection in the past. [9][10][11][12] We have previously reported on the outcome of the German HCV (1b)-contaminated anti-D cohort at 20 and 25 years after infection and demonstrated a very low cirrhosis rate of only 0.5% in the overall cohort at 25 years after infection. 11,12 The aim of the present 35-year followup study was to reevaluate the liver disease progression in this unique cohort after another decade of data accrual in our prospective, community-based, multicenter study.…”

mentioning

confidence: 96%

Evaluation of liver disease progression in the German hepatitis C virus (1b)-contaminated anti-D cohort at 35 years after infection

Wiese¹,

Fischer

Löbermann

et al. 2013

Hepatology

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The natural course of HCV infection remains controversial. The German HCV (1b)-contaminated anti-D cohort provides an ideal population to investigate the natural course of HCV infection in a large, homogenous cohort of young women from the date of HCV inoculation. Our previous follow-up studies at 20 and 25 years after infection suggested slow fibrosis progression rates in this unique cohort. The aim of our prospective, community-based, multicenter study was to reevaluate the liver disease progression in 718 patients of the original anti-D cohort at 35 years after infection. Patients with self-limited HCV infection (n 5 189) were compared to those who failed to eliminate the virus spontaneously (n 5 529), comprising patients who were treatment na€ ıve (n 5 197) or achieved a sustained virological response (SVR; n 5 149), respectively, failed to clear the virus (non-SVR; n 5 183) after antiviral therapy. In the overall cohort, 9.3% of patients showed clinical signs of liver cirrhosis at 35 years after infection. Liver disease progression largely depended on HCV infection status. The highest proportion of patients with clinical signs of end-stage liver disease was observed in the non-SVR group (15.3%), whereas decreased cirrhosis rates were detected in the SVR group (6%) and in patients with self-limited HCV infection (1.1%; P 5 6.2 3 10 26 ). Overall survival was significantly enhanced after SVR, compared to treatment-na€ ıve patients or non-SVR (P 5 0.027). Conclusion: The present study provides further evidence for a mild, but significant, disease progression at 35 years after infection in the German HCV (1b)-contaminated anti-D cohort. Patients with self-limited HCV infection or SVR after antiviral treatment were protected from progressive liver disease and showed the best clinical long-term outcome. (HEPATOLOGY 2014;59:49-57) H epatitis C virus (HCV) infection is the leading cause of end-stage liver disease (ESLD) in the world and represents a major burden for national health systems. 1 The World Health Organisation (WHO) and international consensus conferences refer to the high chronification rate of HCV infection, the risk of subsequent HCV-related complications, including end-stage liver cirrhosis and hepatocellular carcinoma (HCC) and the high costs for antiviral therapy, respectively, liver transplantation (LT). 2,3 It is estimated that HCV-related morbidity and mortality will increase in the next decade. [4][5][6] The predicted cumulative probability of cirrhosis approximates 20% at 20 years after HCV infection and

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“…Indeed, studies of women who were accidentally infected with the same inoculum (contaminated immunoglobulin D antibody) showed that despite receiving the same virus strain, viral diversity could not account for the dichotomy in outcome (clearance versus persistence). [29][30][31][32][33] Thus, differences in the host response were more likely to be the determining factor. Several important insights into this crossroad of viral and host genetics have been forthcoming from studies in human immunodeficiency virus (HIV) infection.…”

Section: Introductionmentioning

confidence: 99%

Impact of the genetic restriction of virus-specific T-cell responses in hepatitis C virus infection

Thimme

2007

Genes Immun

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The immunobiology of hepatitis C virus (HCV) is significantly influenced by the host immune response to the virus, especially by virus-specific T-cell responses. Virus-specific T cells are restricted by human leucocyte antigen class I and II molecules. Of note, associations between these polymorphic loci and outcome and course of HCV infection have been reported in large and well-documented cohorts. This review will briefly summarize these studies and focus especially on the immunological and virological basis for the reported associations. The outcome and course of HCV infection is most likely determined by a complex interplay of genetic, immunological and virological factors. A better understanding of these host-virus interactions is essential not only to gain better insights into the mechanisms of viral clearance and persistence but also for the development of new antiviral vaccine strategies.

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The natural course of hepatitis C virus infection after 22 years in a unique homogenous cohort: spontaneous viral clearance and chronic HCV infection

Cited by 141 publications

References 51 publications

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

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

Evaluation of liver disease progression in the German hepatitis C virus (1b)-contaminated anti-D cohort at 35 years after infection

Impact of the genetic restriction of virus-specific T-cell responses in hepatitis C virus infection

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