In the treatment of chronic hepatitis B with pegylated interferon, ALT (glutamate aminotransferase) levels are one of the most important factors affecting the outcome. A high baseline ALT level also predicts a good response to interferon therapy. However, some patients have expressed concern: if transaminase levels remain high during interferon therapy, or if transaminase levels rise rather than fall during therapy, will this cause damage to the liver? We will first understand the two ways of virus clearance within the liver cells: 1. Lymphocyte clearance: there are many types of lymphocytes, one of which is T cells that are specialized for hepatitis B virus, attacking the hepatitis B virus-infected liver cells, liver cell damage that causes transaminases to be released, which leads to hepatitis, T lymphocytes kill the virus and also destroy the liver cells, so that the cells and the virus die together. 2, inflammatory factor clearance: lymphocytes can also release a variety of inflammatory factors that can enter the liver cells to kill the virus, without having to destroy the liver cells, and the inflammatory process also releases transaminases. The above two ways of clearing the virus have inflammation occurring and making the transaminases increase. So how does interferon clear the virus? Interferon is also an inflammatory factor, and lymphocytes also produce interferon during hepatitis attacks to participate in the inflammatory response. The treatment of chronic hepatitis B with artificially prepared interferon greatly enhances the body’s immune clearance of the hepatitis B virus. In fact, interferon only enhances the body’s immune (inflammatory) response on top of the existing one; if in a chronic carrier state without inflammation, interferon injections alone do not obtain the efficacy of virus clearance. This viral clearance by the action of inflammatory factors does not damage liver cells. So, how high does the transaminase rise during interferon therapy to damage hepatocytes? Interferon treatment for hepatitis is not only involved in the immune response; it is more likely to stimulate the immune response, and if stimulated excessively, generates a large number of multiple inflammatory factors that may make the inflammatory response go out of control. Glutathione can spike to more than ten times the normal high value, and in a few cases, jaundice and even acute liver failure can occur. There is a 10% incidence in the early stages of interferon therapy, which is a more severe adverse reaction and can have exacerbation of the lesion. Therefore, interferon needs to be in the inflammatory environment of the liver in order to fully stimulate the immune effect. If the ALT level exceeds 7 to 8 times the normal high value (40 U/L) there is no damage to the liver; only when it exceeds 10 times is it an adverse reaction to interferon and only then is it necessary to reduce the dosage or stop interferon and give liver-protective and enzyme-lowering treatment. However, to be on the safe side, it is recommended to do liver function tests every month.