Hepatitis B virus infection can be divided into the immune tolerance phase, the immune clearance phase and the inactive or low (non) replication phase. Liver inflammation is not mainly caused by direct viral damage to hepatocytes, but by viral stimulation of the body’s immune response and immune dysfunctional regulation. The pathogenesis of hepatitis B is complex, but has not been fully elucidated to date. It is currently believed that its hepatocellular damage is not the result of HBV replication in hepatocytes, but is mediated by T-cell toxic responses. HBV infection in humans induces cellular and humoral immune responses, and stimulates autoimmune responses and immune regulatory dysfunction. These immune responses are important for the clinical manifestation and regression of hepatitis B. In acute hepatitis, when the immune function is normal, after infection with HBV, the cytotoxic T cells (Tc cells) attack the infected hepatocytes, and the HBV released into the blood by the destroyed hepatocytes is bound by specific antibodies, and more interferon is produced, resulting in the clearance of HBV, and the disease improves and eventually heals. Chronic active hepatitis is seen in people with defective immune function and disorders of immune regulation. After infection with HBV, some hepatocytes are damaged due to abnormal function of Tc cells or specific antibodies that block some hepatocyte target antigens and restrict the T-cell toxic response. Interferon production is low and HBV continues to replicate. Insufficient formation of specific antibodies, hepatocytes are repeatedly invaded by HBV, resulting in chronicity of infection. In addition, hepatocyte membrane-specific lipoproteins (Lsp) form autoantigens due to HBV infection, stimulating B cells to produce anti-Lsp (IgG type), and autoimmune ADCC effects cause progressive hepatocyte damage in the presence of reduced suppressive T cell (Ts cell) activity. Chronic prolonged hepatitis and asymptomatic HBsAg carriers who are infected with HBV when the body is immunocompromised cannot produce an effective immune response, resulting in mild or no hepatocellular damage. Especially asymptomatic HBeAg carriers, lack of interferon, can not clear the virus, resulting in long-term carriage of HBV. Acute heavy hepatitis occurs due to the body’s immune response is too strong, rapid destruction of a large number of HBV-infected hepatocytes in the short term T-cell toxic reaction; or the formation of a large number of antigen-antibody complexes in the short term, activating complement, resulting in a local hypersensitivity reaction (Arthus reaction), resulting in large blocks of The absorption of intestinal-derived endotoxin can lead to Schwartzman reaction, causing ischemic necrosis of hepatocytes; plus cytokines such as alpha-tumor necrosis factor (TNF-α), IL-1 and leukotrienes are released by mononuclear macrophages, promoting hepatocyte injury. The pathogenesis of subacute severe hepatitis is similar to that of acute severe hepatitis, but progresses more slowly. The pathogenesis of chronic severe hepatitis is more complex and needs to be further investigated.