Causes HCV is a group of hepatitis viruses transmitted hematogenously, and was first cloned by Chiron Corporation in the United States in 1989 using molecular cloning techniques. HCV is an RNA virus, which is easily mutated, and only 68.1%-91.8% of the nucleotides of isolates from different regions are identical. At present, there are 8 types of HCV genotypes, and each type has many subtypes. The genotypes distributed in China are mainly type 1b, and a few are type 2a and 2b. Pathogenesis 1, the direct pathogenic role of HCV infection Many studies have shown that the severity of liver tissue inflammation in HCV-infected patients is related to their viraemia. The severity of liver tissue inflammation in patients with chronic hepatitis C correlates more strongly with intracellular HCV RNA levels than it does with serum HCV RNA levels. After treatment with interferon, the serum level of ALT decreased gradually with the decrease of HCV RNA level in serum, and the above results suggest that there may be a direct pathogenic effect of HCV. 2, cell-mediated immune damage may be the main cause of liver lesions caused by HCV One of the important features of hepatic histopathology of hepatitis C is the clustering of lymphocytes in the confluent area, sometimes lymphoid follicles can be formed, and comparative studies suggest that it is more obvious than in hepatitis B. Lymphocyte infiltration is undoubtedly related to the immune response. The E1 and E2/NS of HCV RNA are highly variable regions, which are easily mutated in vivo and can lead to changes in the target antigen (E1 and E2/NS proteins) determinant clusters of the hepatocyte membrane in HCV-infected patients, and Tc cells then recognize the newly emerged antigenic determinant clusters again and attack and destroy the hepatocytes, which is the reason why the higher the rate of HCV RNA mutation, the more severe the inflammation of their liver tissue. It also indicates that immune-mediated mechanisms play an important role in hepatocyte injury in chronic HCV-infected patients. 3. Autoimmunity HCV infected patients often have the following features ① non-specific immune disorders, such as mixed condyloglobulinemia, dry syndrome and thyroiditis; ② non-specific autoantibodies can be detected in serum, such as rheumatoid factor, anti-nuclear antibody and anti-smooth muscle antibody; ③ some type II autoimmune hepatitis [anti-liver and kidney microsomes type I antibody (anti-C-LKM-1 antibody) positive] can appear anti-HCV positivity; ④ anti-GOR may be present; ⑤ Histological changes in the liver are similar to autoimmune liver disease, so it has been speculated that autoimmune factors may be involved in the pathogenesis of HCV infection. However, the relationship between anti-HCV, anti-LKM-1 and anti-GOR, and their pathogenic significance need to be further studied. 4. The significance of apoptosis in the pathogenesis of hepatitis C The expression of Fas antigen in HCV-infected patients is closely related to the degree of liver tissue necrosis and inflammation, and the expression of HCV core antigen in hepatocytes. It indicates that Fas-mediated apoptosis is one of the forms of HCV-infected hepatocyte death. The pathogenesis of HCV infection is complex, and many factors and their interrelationships remain to be further studied and elucidated. Compared with other types of hepatitis, hepatitis C has its characteristic pathological changes 1. Lymphocytes in the confluent area accumulate and can form lymphoid follicles; bile duct epithelial cells degenerate and are surrounded by a large number of lymphocyte infiltrates. Such severe inflammation in the confluent area and bile duct damage are important signs of chronicity of hepatitis C. 2, inflammatory cell infiltration in the hepatic sinusoids, but does not affect the perisinusoidal hepatocytes, this is distinguished from acute hepatitis B, which is often accompanied by eosinophilic degeneration or necrosis of perisinusoidal cells in the etiology of hepatitis B. 3, hepatocyte degeneration and necrosis within the liver lobules are less severe. 4, perisinusoidal and interstitial hepatocellular fibrosis is more pronounced than in hepatitis B, and outlook is earlier. This may be one of the reasons why it is more likely to develop into hepatic steatosis. 5, Hepatocellular steatosis is common.