China is a highly endemic area for hepatitis B virus infection, with the rate of hepatitis B virus infection close to 60% and the rate of hepatitis B virus surface antigen positivity close to 10%. In the treatment of hepatitis B, many patients simply believe that a negative index is a sign of improvement, so they use the so-called “negative” drugs at any cost, resulting in money spent, but the condition is even worse. Can hepatitis B indicators actually turn negative? How should I look at a negative hepatitis B indicator? It should be said that after standardized antiviral treatment, it is possible to achieve certain hepatitis B virus indicators to turn negative. According to the current treatment conditions, there are four levels of treatment: Level 1: “Basic” goal of conversion is to achieve durable suppression or conversion of HBV DNA (hepatitis B virus deoxyribonucleic acid, which indicates the active level of hepatitis B virus replication) through standardized antiviral treatment. Studies of the natural history of hepatitis B virus infection (10+ years of long-term follow-up) have shown that higher HBV DNA serum levels are associated with a higher risk of cirrhosis and primary liver cancer. In general, about 3% to 4% of people with serum HBV DNA ≥ 106 copies/ml may develop cirrhosis each year (36.2% of infected people develop cirrhosis after 10 years) and about 1% to 2% may develop liver cancer (14.89% of infected people develop primary liver cancer after 10 years). Therefore, the basic or primary goal of antiviral therapy for chronic hepatitis B patients, whether HBeAg-positive or negative, is to achieve a durable conversion of HBV DNA. The longer the duration of such transitions, the better, suggesting that the hepatitis B virus is durably suppressed, will reduce or prevent the occurrence of cirrhosis and hepatocellular carcinoma. The second level: “satisfactory” conversion target is mainly for HBeAg-positive chronic hepatitis B patients to achieve sustained HBeAg conversion or serologic conversion (HBeAg conversion and anti-HBe conversion) through standardized antiviral therapy to improve the prognosis of chronic hepatitis B. Long-term follow-up studies of hepatitis B virus-infected patients have also shown that the incidence of cirrhosis and primary liver cancer is significantly higher in those who are positive for both HBsAg and HBeAg than in those who are positive for HBsAg alone and negative for HBeAg. Therefore, for HBeAg-positive chronic hepatitis B patients, on the basis of achieving durable HBV DNA conversion, it is very important to further achieve durable HBeAg conversion or serological conversion to stop or delay the occurrence and development of cirrhosis and hepatocellular carcinoma. Moreover, the presence of HBeAg is the underlying cause of chronicity of hepatitis B virus infection and inhibits the immune clearance of hepatitis B virus by the body’s immune system. Therefore, achieving HBeAg conversion or serological conversion is both an immune control process and an important sign of remission. Not only is the level of HBV DNA replication significantly reduced in the body, but there will also be improvement in liver function and significant improvement in liver tissue inflammation, and furthermore, there will be gradual improvement or even reversal of liver fibrosis. The third level: the “ideal” conversion goal is to achieve durable HBsAg conversion or serological conversion (HBsAg conversion and anti-HBs conversion) in chronic hepatitis B patients (including HBeAg-positive and HBeAg-negative patients) through standardized antiviral therapy, which marks the improvement of liver tissue inflammation and fibrosis or reversal, and improved long-term prognosis. However, this ideal goal of conversion is difficult to achieve under realistic conditions, and the current antiviral drugs (including nucleoside analogues and interferons) are not ideal, and even interferon therapy is likely to achieve sustained HBsAg conversion or serological conversion in only about 10% of patients with chronic hepatitis B. The duration of treatment must be at least 1 year. In fact, there is no need to deliberately pursue this “ideal” goal of conversion under the current realistic conditions, and the rumored “full conversion of major and minor triplets” is undoubtedly deceptive. In addition, it should be noted that even if the “ideal” goal is achieved, it does not mean that the hepatitis B virus is completely cleared from the body of the chronic hepatitis B patient, and there are still very few patients who still have potential or low levels of viral replication in their liver tissue. The fourth level: the “ultimate” goal of conversion Through standardized antiviral treatment, the hepatitis B virus covalent closed-loop DNA (HBV cccDNA, which is the template of hepatitis B virus replication in liver cells) in the nucleus of chronic hepatitis B patients is converted to negative or cleared, which means that the hepatitis B virus in the body of chronic hepatitis B patients has been completely cleared This means that the hepatitis B virus has been completely cleared from the body of the chronic hepatitis B patient and that the patient is completely free from the hepatitis B virus infection, which is a true cure. This is the ultimate goal, and claims of a complete cure for hepatitis B are, of course, empty words and lies. The actual “panacea” for chronic hepatitis B. There are two main types of medications, namely interferon and nucleoside (acid) drugs. Interferon includes regular interferon, pegylated interferon and albumin interferon (which may enter the country in 1 to 2 years), while nucleoside drugs include lamivudine, adefovir, entecavir, tipivudine and tenofovir, emtricitabine, etc., which have not yet entered the country. Patients with chronic hepatitis B should choose the right time and the right drug for treatment under the guidance of a specialist and according to their specific condition and previous treatment, and adjust the treatment regimen and determine the appropriate course of treatment according to their response to treatment, and standardize antiviral therapy. As for herbal treatment and gene therapy and cell therapy, two points need to be clarified: first, herbal medicine, its anti-fibrotic and immunomodulatory effects are certain, but its antiviral efficacy is inaccurate; second, the so-called hepatitis B gene therapy, cell therapy, due to its many outstanding issues, especially the potential long-term impact on the human body and safety is still unclear, whether the U.S. FDA, the European Union, or China’s National Food and Drug Administration (FDA). The EU and the State Food and Drug Administration have not approved the clinical treatment of chronic hepatitis B. As for some false advertisements boasting of the so-called “hepatitis B to negative king”, “hepatitis B nemesis”, “gene therapy to quickly turn negative” and other so-called “panacea The “Hepatitis B” is not only unknown, the mechanism of action is unclear, and without strict clinical trials of drug registration to assess its efficacy and safety, it is unauthorized for human treatment, should be illegal.