Abstract
AimCellular CD81 is a well characterized hepatitis C virus (HCV) entry factor, while the relevance of soluble exosomal CD81 in HCV pathogenesis is poorly defined. We performed a case-control study to investigate whether soluble CD81 in the exosomal serum fraction is associated with HCV replication and inflammatory activity.Patients and MethodsFour cohorts were investigated, patients with chronic hepatitis C (n = 37), patients with chronic HCV infection and persistently normal ALT levels (n = 24), patients with long term sustained virologic response (SVR, n = 7), and healthy volunteers (n = 23). Concentration of soluble CD81 was assessed semi-quantitatively after differential centrifugation ranging from 200 g to 100,000 g in the fifth centrifugation fraction by immunoblotting and densitometry.ResultsSoluble CD81 was increased in patients with chronic hepatitis C compared to healthy subjects (p = 0.03) and cured patients (p = 0.017). Patients with chronic HCV infection and persistently normal ALT levels and patients with long term SVR had similar soluble CD81 levels as healthy controls (p>0.2). Overall, soluble CD81 levels were associated with ALT levels (r = 0.334, p = 0.016) and severe liver fibrosis (p = 0.027).ConclusionCD81 is increased in the exosomal serum fraction in patients with chronic hepatitis C and appears to be associated with inflammatory activity and severity of fibrosis.
Highlights
Chronic hepatitis C virus (HCV) infection is a major cause of liver cirrhosis, and hepatocellular carcinoma worldwide [1,2]
Soluble CD81 was increased in patients with chronic hepatitis C compared to healthy subjects (p = 0.03) and cured patients (p = 0.017)
CD81 is increased in the exosomal serum fraction in patients with chronic hepatitis C and appears to be associated with inflammatory activity and severity of fibrosis
Summary
Chronic hepatitis C virus (HCV) infection is a major cause of liver cirrhosis, and hepatocellular carcinoma worldwide [1,2]. The protease inhibitors boceprevir and telaprevir, which are associated with considerably enhanced sustained virologic response (SVR) rates in HCV genotype 1 infected patients in combination with pegylated interferon-alfa and ribavirin, have been approved by the European Medicines Agency and the Food and Drug Administration [3,4,5]. Approximately one quarter of patients with HCV genotype 1 infection are assumed not to achieve SVR even with triple therapy including either boceprevir or telaprevir [6]. Cell entry inhibitors may be useful in prevention of otherwise inevitable graft infection after orthotopic liver transplantation in HCV associated liver cirrhosis and hepatocellular carcinoma. Proof-of-concept studies suggest that the new class of HCV entry inhibitors has a substantial capability to widen preventive and therapeutic options in HCV infection [11]
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