Hepatitis C virus
1974 Golafield first report of post-transfusion non-A non-B hepatitis. 1989 Choc applications such as molecular cloning techniques to obtain the viral gene cloning, and named the disease and the virus is hepatitis C (Hepatitis C) and hepatitis C virus (HCV). As the HCV genome and phenotypic characteristics of the structure with the yellow virus and plague virus were similar to their classified as Flaviviridae HCV.
European and American countries are now the majority of known HCV-Ⅰ infection, while Asian countries the main type Ⅱ, Ⅲ type followed. Okomoto report Japanese chronic hepatitis C patients and healthy blood donors is mainly Ⅱ infection, accounting for 59.3% and 82.4%, while about 50% of hemophiliacs were infected with type Ⅰ, because the application enter the United States imported coagulation factor Ⅷ. Wang’s report on China’s Beijing in patients with chronic hepatitis C infection of 86.2% as type Ⅱ, Ⅲ infection of 13.8%. Infection in patients with type Ⅲ and the Xinjiang accounts for 50%, indicating different types of HCV have a certain distribution of the places and people. In addition, the clinical course of infection of different genotypes and response to interferon treatment is also shown in different clinical symptoms of infection, such as type Ⅲ heavier, there is tendency to rise to severely punish the liver: Ⅱ model (Simmonds 1b) infection on interferon therapy is not sensitive to poor results. Ⅲ infection (Simononds 2a) good results with interferon therapy.
Pathogenicity and immunity
Source of infection with hepatitis C is mainly acute clinical and subclinical asymptomatic patients, chronic patients and HIV carriers. Most patients for 12 days prior to the onset, the blood that is infectious and can be carriers of the virus over 12 years. The main source of HCV spread of blood, 30-90% of foreign post-transfusion hepatitis of hepatitis C, our post-transfusion hepatitis Hepatitis C accounts for 1 / 3. As well as through other means, such as vertical transmission, the family daily contacts and sexual propagation.
Enter with HCV or HCV-RNA in plasma or blood products, usually after 6-7 weeks incubation period of cases of acute onset, clinical manifestations general weakness, poor appetite, liver discomfort, 1 / 3 of patients have jaundice, ALT increased, anti-HCV antibodies. 50% of clinical hepatitis C patients may develop chronic hepatitis, and even some patients may lead to liver hard and hepatocellular carcinoma. The rest, about half of the patients as self-limiting, automatic recovery.
Pathogenesis of hepatitis C has not yet fully clear, when the HCV replication in liver cells caused by structural and functional changes of liver cells, or interfere with liver cell protein synthesis, can cause liver cell degeneration and necrosis, indicating that HCV directly damage the liver, leading to disease play a role. However, most scholars believe that the cellular immune response may play an important role in pathology and found that, like hepatitis C and hepatitis B and its tissue infiltration by CD3 + cells, mainly cytotoxic T cells (TC)-specific attack on HCV infection of target cells, can cause liver cell injury.
Clinical observations show that people are infected with HCV after the protective immunity generated by poor, longer infected with different, and even some patients lead to cirrhosis and hepatocellular carcinoma. The rest, about half of the patients as self-limiting, automatic recovery.
Pathogenesis of hepatitis C has not yet been very clear, when the HCV replication in liver cells caused by structural and functional changes of liver cells, or interfere with liver cell protein synthesis, can cause liver cell degeneration and necrosis, indicating that HCV directly damage the liver, leading to play a role in pathogenesis . But most of mathematics that the cellular immune response may play an important role in pathology and found that, like hepatitis C and hepatitis B and its tissue infiltration by CD3 + cells, mainly cytotoxic T cells (TC)-specific attack on HCV infection of target cells, can cause liver cell injury.
Clinical observations show that people are infected with HCV after the protective immunity generated by poor, longer infected by different strains, and even the same strain of HCV. HCV infection may be related to the low level of viremia and the HDV-level variation of sex-related genes.