Chronic hepatitis B “positive to negative” treatment objectives

I. About the hepatitis B surface antigen conversion “HBsAg (surface antigen) positive to negative”, why is it “difficult to achieve”? It is true that, so far, no one in the world’s medical doctors dare to say that there is a drug to make HBsAg turn negative. I was a visiting scholar in the U.S. and asked for advice on this issue, and the answer I got was “I am sorry”. The implication is that I can’t answer your question because it is very difficult to turn surface antigen positive. The consensus among experts is that HBsAg is a protein shell on the surface of the hepatitis B virus, which is not infectious and has no effect on the body (the hepatitis B vaccine is made from it). But why is it said that it is the sign of “complete cure of hepatitis B”, because it is the shell and traces of the hepatitis B virus, as long as there is the hepatitis B virus, then it will leave traces, after the hepatitis B virus is completely destroyed, HBsAg will also slowly turn negative. This fortress will eventually be conquered by humans, but for now it is difficult. The actual HBV-DNA is a key point in the treatment of hepatitis B, because it is a sign that the hepatitis B virus has stopped replicating. If the HBV-DNA can turn negative for a long time, then it is very beneficial to the human body, even if the HBsAg is still positive, the effect is very weak. At present, there are more and more means to make “HBV-DNA positive to negative” and the efficacy is improving, please refer to the relevant chapters in this book. About e antigen positive to negative About “HBeAg (e antigen) positive”, HBeAg, as a viral antigen, can be considered as one of the important structures of hepatitis B virus, positive indicates that the virus is more active, is replicating, and has a strong infectious. It is the real target of hepatitis B conversion treatment, as well as HBV-DNA. Anti-viral therapy is used to promote its conversion and preferably “serological conversion”, i.e. HBeAg conversion and anti-HBe (e antibody) conversion, and if serological conversion does not occur, there is a high probability of HBeAg conversion again. The results of a clinical study on long-acting interferon piroxin for HBeAg-positive hepatitis B showed that HBeAg seroconversion in patients was more important than HBV-DNA inhibition, and patients who did not achieve HBeAg seroconversion by HBV-DNA inhibition alone were still at risk of relapse. Therefore, seroconversion of e antigen (i.e., conversion from e antigen positive to e antibody positive) is the focus of treatment in clinical therapy. IV. About the conversion of anti-HBe and anti-HBc About the conversion of anti-HBe and anti-HBc (see Chapter 4, Section 2 of this book), since neither is a component of the virus itself, conversion is meaningless. In particular, anti-HBe, as mentioned earlier, is a marker of serological conversion of e antigen, which many experts use as one of the clinically valid indicators, not to mention conversion to negative. In conclusion, it is now internationally recognized that the goal of treatment for chronic hepatitis B is to remove or durably suppress the hepatitis B virus and delay its evolution to cirrhosis and primary liver cancer. Therefore, when talking about conversion, do not go into the “conversion misunderstanding”, but have the correct purpose of conversion.