Hepatitis C virus (HCV) infects an estimated 180 million persons worldwide and it is the cause of most cases of hepatitis in the world, and the principal cause of chronic liver disease, cirrhosis (end stage of scarring process of the liver), and primary liver cancer which is termed hepatocellular carcinoma. Hepatitis C virus was first recognized in 1975 and named non-A non-B hepatitis virus.
After the virus genome was sequenced, it was renamed HCV.
Hepatitis C is an increasing public health concern in the United States and throughout the world. HCV is one of the most common causes of chronic liver disease in the United States and the most common cause of chronic viral hepatitis. About 4 million people in the United States have antibodies to HCV, meaning they have been infected with the virus at some point;
as many as half of them haven't known yet they have contracted the infection.
The majority of HCV infections become chronic, but the progression of disease associated with HCV is highly variable. Chronic hepatitis C (CHC) can progress slowly as asymptomatic hidden disease and end in liver failure 10-15-20 years later. There is no vaccine and conventional treatment options are limited.
All current conventional treatments are based on synthetic interferon-alpha. Many people who become HCV-infected are immediately excluded from this treatment because of contraindications to interferon. Of the group than can take interferon, many will not respond to treatment; or they will respond and then relapse.
The success rate of retreatment with interferon-alpha is so low.
Hepatitis C virus infection results in an increased expression of profibrogenic (i.e. stimulating fibrosis) factors in infected hepatocytes and neighboring cells.
The direct induction of profibrogenic mediators by hepatitis C virus in infected hepatocytes explains the frequent observation of progressive liver fibrosis despite a low level of liver inflammation. Besides the chronic viral infection determinants of fibrosis progression include both environmental and genetic factors.
The major hepatological consequence of HCV infection is the progression to cirrhosis and its life-threatening complications. Several factors have been clearly shown to be associated with fibrosis progression rate:
- age at infection
- duration of infection,
- male gender,
- consumption of alcohol,
- HIV or HBV coinfection,
- low CD4 T-cells count
As age and duration of infection increases, the risk of fibrosis increases and the impact of conventional treatment decreases. In conclusion, fibrosis progression has a progressive acceleration, and gender, age and consumption of alcohol are strongly involved in this progression.
Our six year clinical experience shows that recurring transplantations of cultured hepatoblasts (cell therapy) prevent progression of HCV infection to cirrhosis and result in significant reversal of preexisting cirrhosis. In some cases combination treatment is applied (i.e. cell therapy plus medical treatment and immunotherapy).
Synonyms and related keywords: hepatitis C virus, HCV, HCV
infection, HCV-infection, non-A non-B hepatitis, NANB hepatitis,
acute hepatitis, hepatitis, virus infection, viral infection, virus,
chronic liver disease, hepatocellular carcinoma, hepatoma, HCC,
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OLT, interferon, IFN, sustained virological response, HIV-HCV coinfection,
HIV-HCV co-infection, IFN therapy, interferon therapy, pegylated
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hronic hepatitis C, liver failure, interferon-alpha, interferon, hepatitis C virus infection, HCV infection, fibrosis, progressive liver fibrosis,
liver fibrosis, treatment, contraindications, transplantations of cultured hepatoblasts, cultured hepatoblasts, cell therapy, hepatocellular carcinoma, liver cancer, hepatocyte transplantation, cultured hepatocyte transplantation, liver cell transplantation,
hepatoblast transplantation, cultured hepatoblast transplantation